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Bozkurt, Süreyya, Filiz Yarimcan, Hüseyin Ayhan, et al. "Investigation of PTGS2, MAGE-A3, CALR, KRT19 and TMPRSS4 expressions in HCT116 colon cancer and PC3 prostate cancer cell lines." Genetics & Applications 4, no. 2 (2020): 37. http://dx.doi.org/10.31383/ga.vol4iss2pp37-42.
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Cancer is a disease arising from DNA alterations that dysregulate gene structure and function. These deregulated genes can also play a role in tumor invasion and metastasis or resistance to treatment. In this study, we determined the gene expression during transcription of PTGS2 (Prostaglandin-endoperoxide synthase 2), MAGE-A3 (Melanoma-associated antigen 3), CALR (Calreticulin), KRT19 (Cytokeratin 19), and TMPRSS4 (Transmembrane protease, serine 4) in HCT116 colon cancer cell line and PC3 prostate cancer cell line. After RNA isolation and cDNA conversion, DNA amplification was performed with Real-Time PCR. We determined the altered transcriptional expression level of those genes. In HCT116 colon cancer cell line, expression of the TMPRSS4 gene, MAGEA3 gene and KRT19 gene was found as increased and expression of the CALR gene and the PTGS2 gene was found as decreased. Especially a 93.70-fold increase in expression of the KRT19 gene was found in HCT116 colon cancer cell line. In PC3 prostate cancer cell lines, TMPRS4 gene expression and MAGEA3 gene expression were found as increased. But there was 50 fold decrease in PTGS2 gene expression.
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Tran, Phuong Linh, and Khac Cuong Bui. "DNA-DEPENDENT PROTEIN KINASE INHIBITOR INDUCES APOPTOSIS IN COLON CANCER CELLS." VietNam Military Medical Unisversity 49, no. 4 (2024): 22–32. http://dx.doi.org/10.56535/jmpm.v49i4.726.
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Objectives: Among all types of DNA damage, DNA double-strand breaks (DSBs) are considered the most deleterious form induced by either endogenous factors (oxi-dative damages, mismatches, altered chromatin structures, and missing, or modified nucleotides) or exogenous factors, i.e., ultraviolet (UV) radiation, ionizing radiation (IR), and chemicals or drugs. DNA-dependent protein kinase (DNA-PK) plays a crucial role in repairing DSBs through non-homologous end joining (NHEJ). Cells lacking DNA-PK exhibit heightened sensitivity to IR and various DNA-damaging agents. The inhibition of DNA-PK further intensifies cellular susceptibility to IR and DNA-damaging agents. Several small molecules that inhibit DNA-PK have been developed. This study aimed to evaluate the effect of DNA-PK inhibitor (DNA-PKi) NU7441 on the HCT116 cell line. Methods: DNA-PKi NU7441 was used to assess the effect on anti-proliferation and induction of apoptosis on the HCT116 colorectal cancer cell line. Cells were cultured under standard conditions; crystal violet and apoptosis assay were applied to evaluate cell proliferation and apoptosis. Data were analysed using GraphPad Prism 8.4. Results: DNA-PKi effectively inhibited HCT116 colon cancer cell growth via crystal violet assay (p < 0.01). In addition, DNA-PKi also induced programmed cell death in the HCT116 cell line (p < 0.05). Conclusion: DNA-PKi NU7441 suppressed cell proliferation and induced apoptosis in the HCT116 colon cancer cell line.
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Luo, Ping, Shugui Wu, Kaibao Ji, et al. "LncRNA MIR4435-2HG mediates cisplatin resistance in HCT116 cells by regulating Nrf2 and HO-1." PLOS ONE 15, no. 11 (2020): e0223035. http://dx.doi.org/10.1371/journal.pone.0223035.
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Purpose Cisplatin resistance is still a serious problem in the clinic. However, the underlying mechanism remains unknown. In our study, we investigated cisplatin resistance by using the cisplatin-resistant cell line HCT116R. Methods The HCT116 cell line, a colon cancer cell line, was purchased. Cell viability was determined using CCK-8 Assay Kit. The gene expression levels of MIR4435-2HG, Nrf2, and HO-1, and caspase activity were determined using qRT-PCR and Caspase 3 Assay Kit, respectively. Results In this study, we found that the levels of the lncRNA MIR4435-2HG were dramatically increased in the cisplatin-resistant cell line HCT116R. Knockdown of MIR4435-2HG in HCT116R cells significantly restored the sensitivity to cisplatin, inhibited cell proliferation and promoted cell apoptosis. Furthermore, Nrf2 and HO-1 mRNA levels, as critical molecules in the oxidative stress pathway, were inhibited by siRNAs targeting MIR4435-2HG, suggesting that MIR4435-2HG-mediated cisplatin resistance occurs through the Nrf2/HO-1 pathway. Conclusion Our findings demonstrate that the lncRNA MIR4435-2HG is a main factor driving the cisplatin resistance of HCT116 cells.
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Pan, Jie, Zongbin Xu, Meifang Xu, Xiaoyan Lin, Bingqiang Lin, and Mengxin Lin. "Knockdown of Forkhead box A1 suppresses the tumorigenesis and progression of human colon cancer cells through regulating the phosphatase and tensin homolog/Akt pathway." Journal of International Medical Research 48, no. 12 (2020): 030006052097145. http://dx.doi.org/10.1177/0300060520971453.
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Background This study aimed to evaluate the role and the underlying mechanisms of Forkhead box A1 (encoded by FOXA1) in colon cancer. Methods We analyzed FOXA1 mRNA and protein expression in colon cancer tissues and cell lines. We also silenced FOXA1 expression in HCT116 and SW480 cells to evaluate the effects on cell proliferation, cell cycle, migration, and invasion by using MTT, colony formation, flow cytometry, and the Transwell assay, respectively. Results FOXA1 immunostaining was higher in colon cancer tissues than adjacent healthy tissues. FOXA1 mRNA and protein expression was significantly increased in human colon cancer cells compared with a normal colonic cell line. FOXA1 expression was also significantly higher in colorectal cancer tissues from TCGA data sets and was associated with worse prognosis in the R2 database. FOXA1 expression was negatively correlated with the extent of its methylation, and its knockdown reduced proliferation, migration, and invasion, and induced G2/M phase arrest in HCT116 and SW480 cells by suppressing the phosphatase and tensin homolog/Akt signaling pathway and inhibiting epithelial–mesenchymal transition. Conclusion FOXA1 may act as an oncogene in colon cancer tumorigenesis and development.
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Li, Yanchu, Rong Pu, Lu Zhou, Dan Wang, and Xianyong Li. "Effects of a Chlorogenic Acid-Containing Herbal Medicine (LASNB) on Colon Cancer." Evidence-Based Complementary and Alternative Medicine 2021 (August 20, 2021): 1–12. http://dx.doi.org/10.1155/2021/9923467.
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Background. Plant polyphenols, which contain phenolic acids such as chlorogenic acid (CGA), can be used for the treatment of gastrointestinal cancer and have gained increasing attention in recent years. In this study, we explored a novel CGA-containing herbal medicine named LASNB, which was extracted from Lonicera japonica Thunb., Agrimonia eupatoria L., and Scutellaria barbata D.Don. Methods. CGA in LASNB was analyzed using high-performance liquid chromatography (HPLC). The biological functions and molecular mechanisms of LASNB were investigated in colon cancer cell lines (HCT116, HCT15, and CT26), a normal colon cell line (NCM460), and a CT26 xenograft model. To assess safety, hematological toxicity and pathology of the liver, kidney, and lung were evaluated. Results. LASNB suppressed HCT116, HCT15, and CT26 colon cancer progression by inhibiting proliferation capacity, promoting cell apoptosis, and suppressing cell migration both in vitro and in vivo. Investigation into the underlying molecular mechanism indicated that LASNB suppressed the activation of receptor tyrosine kinase- (RTK-) MEK-ERK and NF-κB pathways. With regard to safety, slight interstitial vascular congestion in the lung was observed, but no severe pathological or hematological toxicity was detected. Conclusions. We found that LASNB suppressed the progression of colon cancer via the RTK-MEK-ERK and NF-κB pathways, with no severe toxicity observed. Therefore, LASNB has the potential to be used as a supplementary herbal medicine for the treatment of colon cancer.
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Praphasawat, Ratsada, Sarawoot Palipoch, Prasit Suwannalert, et al. "RED RICE BRAN EXTRACT SUPPRESSES COLON CANCER CELLS VIA APOPTOSIS INDUCTION/CELL CYCLE ARREST AND EXERTS ANTIMUTAGENIC ACTIVITY." Experimental Oncology 45, no. 2 (2023): 220–30. http://dx.doi.org/10.15407/exp-oncology.2023.02.220.
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Background. Red rice bran extract (RRBE) contains many biologically active substances exerting antioxidant and anti-inflammatory effects. Aim. To evaluate the anticancer potential of RRBE in human colon cancer cells and its mutagenic/antimutagenic effects on nonmalignant cells. Materials and Methods. The cytotoxic effect of RRBE was determined by trypan blue exclusion in HCT116, HT29 cell lines and a non-cancerous HEK293 cell line, and its antiproliferative effect using MTS and colony formation assay. The apoptosis induction was evaluated using ELISA, and the apoptotic rate and cell cycle progression were assessed by flow cytometry. The mutagenic/ antimutagenic potential of RRBE was analyzed by micronucleus assay in the V79 cell line. Results. RRBE caused a dose-dependent reduction of cell viability in colon cancer cells and showed a limited cytotoxicity against HEK293 cells. The treatment with RRBE suppressed proliferation of HCT116 and HT29 cells and induced apoptosis as evidenced by the increased DNA fragmentation and the apoptotic cell counts. Furthermore, RRBE treatment significantly increased the number of cells at the G2/M phase triggering the arrest of the cell cycle in colon cancer cells. Interestingly, RRBE did not increase the micronucleus frequency in V79 cells but reduced the micronucleus formation caused by mitomycin C. Conclusion. RRBE effectively suppressed proliferation, induced apoptosis, and caused a cell cycle arrest in human colon cancer cells while being non-mutagenic and exerting antimutagenic effects in vitro.
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Sabit, Hussein, Mariam B. Samy, Osama A. M. Said, and Mokhtar M. El-Zawahri. "Procaine Induces Epigenetic Changes in HCT116 Colon Cancer Cells." Genetics Research International 2016 (October 24, 2016): 1–7. http://dx.doi.org/10.1155/2016/8348450.
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Colon cancer is the third most commonly diagnosed cancer in the world, and it is the major cause of morbidity and mortality throughout the world. The present study aimed at treating colon cancer cell line (HCT116) with different chemotherapeutic drug/drug combinations (procaine, vorinostat “SAHA,” sodium phenylbutyrate, erlotinib, and carboplatin). Two different final concentrations were applied: 3 μM and 5 μM. Trypan blue test was performed to assess the viability of the cell before and after being treated with the drugs. The data obtained showed that there was a significant decrease in the viability of cells after applying the chemotherapeutic drugs/drug combinations. Also, DNA fragmentation assay was carried out to study the effect of these drugs on the activation of apoptosis-mediated DNA degradation process. The results indicated that all the drugs/drug combinations had a severe effect on inducing DNA fragmentation. Global DNA methylation quantification was performed to identify the role of these drugs individually or in combination in hypo- or hypermethylating the CpG dinucleotide all over the genome of the HCT116 colon cancer cell line. Data obtained indicated that different combinations had different effects in reducing or increasing the level of methylation, which might indicate the effectiveness of combining drugs in treating colon cancer cells.
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Farmakovskaya, M. D., N. V. Khromova, B. P. Kopnin, and P. B. Kopnin. "E-CADHERIN EXPRESSION DOWNREGULATION ELEVATES TUMOROGENIC POTENTIAL OF HUMAN COLON CANCER CELL LINE HCT116 VIA INCREASE IN CANCER STEM CELLS AMOUNT." Russian Journal of Biotherapy 15, no. 3 (2016): 6–14. http://dx.doi.org/10.17650/1726-9784-2016-15-3-06-14.
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Introduction. E-cadherin aberrant expression or complete loss is common for a number of human malignant neoplasms, and can be a launching mechanism of an epithelial-mesenchymal transition. Passing through epithelial-mesenchymal transition could in turn promote to the acquisition of so called cancer stem cell phenotype by the transformed cells. The objective of the present study is to reveal the influence of E-cadherin expression level on the amount of cancer stem cells in human colon cancer cell line HCT116. Materials and methods. We have created cell sublines with E-cadherin up- and downregulation and assessed the percentage of cancer stem cells using tumor formation assay, clonogenic assay; we also evaluated profile of cell pluripotency markers. Results and conclusion. We have shown that the proportion of cancer stem cells in human colon adenocarcinoma cell line HCT116 depends on the E-cadherin expression level. E-cadherin expression downregulation results in elevated expression of pluripotency genes and in the increase of proportion of cancer stem cells via activation of Wnt/ß-signalling pathway. E-cadherin upregulation has a reverse effect and decreases the amount of HCT116 cancer stem cells. Thus, E-cadherin expression restoration seems prospective in colorectal anticancer therapy.
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Das, Tanushree, Snehasis Mishra, Sayoni Nag, and Krishna Das Saha. "Green-synthesized gold nanoparticles from black tea extract enhance the chemosensitivity of doxorubicin in HCT116 cells via a ROS-dependent pathway." RSC Advances 12, no. 15 (2022): 8996–9007. http://dx.doi.org/10.1039/d1ra08374k.
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Pasca, Sergiu, Calin Ionescu, David Andras, et al. "Circulating microRNA-194 and microRNA-1228 Could Predict Colon Cancer Proliferation via Phospho S6 Modulation." Journal of Gastrointestinal and Liver Diseases 29, no. 3 (2020): 361–67. http://dx.doi.org/10.15403/jgld-2558.
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Background and Aims: Although colon cancer has a decreasing incidence trend in Europe, because of its still high frequency and not fully understood pathogenesis, this malignancy still remains a subject of intense research. The aim of this study was to investigate the role of microRNA-194 and microRNA-1228 in colon cancer proliferation.
 Methods: RNA was extracted from patients with colon cancer with or without advanced disease and microRNA expression levels were determined through qRT-PCR. Assays were performed on HCT116 cell line and included qRT-PCR, western blotting and cell counting.
 Results: We observed that both microRNAs 194 and 1228 were altered in patients with colon cancer compared with healthy individuals. We observed a lower expression of both microRNA-194 and microRNA-1228 in patients with advanced colon cancer. To validate their pathogenetic role we performed viability and invasion assays on HCT116 cell line transfected with mimics or inhibitors of the mentioned microRNAs, with observable changes in viability and invasion. Furthermore, to determine the altered signaling induced by these microRNAs, we performed western blotting for phospho S6 on HCT116 cells transfected with mimic and inhibitor of the above-mentioned microRNAs with observable differences.
 Conclusion: In the current study we have shown that both microRNA-194 and microRNA-1228 alteration was correlated with the presence of advanced colon cancer, a fact that was further validated in vitro through an invasion assay. Moreover, we have also shown that their effect might be mediated through phospho S6 expression.
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Gwak, Eun, Dasol Kim, Hui-Yun Hwang, and Ho Kwon. "Mitochondrial ROS Produced in Human Colon Carcinoma Associated with Cell Survival via Autophagy." Cancers 14, no. 8 (2022): 1883. http://dx.doi.org/10.3390/cancers14081883.
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Human colon carcinomas, including HCT116 cells, often exhibit high autophagic flux under nutrient deprivation or hypoxic conditions. Mitochondrial ROS (mROS) is known as a ‘molecular switch’ for regulating the autophagic pathway, which is critical for directing cancer cell survival or death. In early tumorigenesis, autophagy plays important roles in maintaining cellular homeostasis and contributes to tumor growth. However, the relationships between mROS and the autophagic capacities of HCT116 cells are poorly understood. Ubiquinol cytochrome c reductase binding protein (UQCRB) has been reported as a biomarker of colorectal cancer, but its role in tumor growth has not been clarified. Here, we showed that UQCRB is overexpressed in HCT116 cells compared to CCD18co cells, a normal colon fibroblast cell line. Pharmacological inhibition of UQCRB reduced mROS levels, autophagic flux, and the growth of HCT116 tumors in a xenograft mouse model. We further investigated mutant UQCRB-overexpressing cell lines to identify functional links in UQCRB-mROS-autophagy. Notably, an increasing level of mROS caused by UQCRB overexpression released Ca2+ by the activation of lysosomal transient receptor potential mucolipin 1 (TRPML1) channels. This activation induced transcription factor EB (TFEB) nuclear translocation and lysosome biogenesis, leading to autophagy flux. Collectively, our study showed that increasing levels of mROS caused by the overexpression of UQCRB in human colon carcinoma HCT116 cells could be linked to autophagy for cell survival.
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Lupidi, Giulio, Massimo Bramucci, Luana Quassinti, et al. "Antiproliferative activities of Artemisia herba-alba ethanolic extract in human colon cancer cell line (HCT116)." Alternative Medicine Studies 1, no. 1 (2011): 14. http://dx.doi.org/10.4081/ams.2011.e14.
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<p><strong></strong><em>Artemisia herba-alba</em> (AHE) is a plant commonly used in traditional medicine for the treatment of various ailments. Here, we investigated the antioxidant and antitumor activity of the aqueous and ethanol extracts of AHE in human colon cancer HCT116 cells. The antioxidant activity was measured by DCFH assay, while antitumor effects were assessed by cell viability assays, cell cycle progression by flow cytometry, and DNA fragmentation analysis in addition to investigating the expression of key cell cycle and apoptotic proteins. While the aqueous extract had no antineoplastic effects, the ethanol extract significantly decreased HCT116 viability (IC50 of 51mg/mL at 24 h) and inhibited the production of reactive oxygen species (ROS). Treatment of HCT116 cells with the ethanol extract also caused dramatic increase in the PreG1 population with concomitant decrease in cycling cells, provoked DNA fragmentation, significant increase in the expression levels of p53 and Bax proteins and activated pro-apoptotic caspase-3. The results obtained suggest that the ethanol extract of AHE could be used as an easily accessible source of natural antioxidants and as potential phytochemicals against colon cancer.</p>
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Pasković, Igor, Mario Franić, Marija Polić Pasković, et al. "Silicon Foliar Fertilisation Ameliorates Olive Leaves Polyphenolic Compounds Levels and Elevates Its Potential towards Different Cancer Cells." Applied Sciences 14, no. 11 (2024): 4669. http://dx.doi.org/10.3390/app14114669.
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It is not yet clear how adding silicon foliar fertilisation affects olive leaf (OL) phenolics and their potential to impact different cancer cells. Thus, we conducted a field trial to study the effect of foliar Si biostimulant fertilisation on the OL phenolic content of the ‘Leccino’ (LE) and ‘Istarska Bjelica’ (IB) cultivars. The experiment compared untreated Control (C) and three distinct levels of silicon (Si1, Si2, Si3) with Si concentrations of 0.55 g/L, 1.1 g/L, and 2.2 g/L, respectively. Si3 application resulted in the highest levels of oleuropein, apigenin-7-O-glucoside, luteolin-4-O-glucoside, rutin, and tyrosol compared to the C treatment. The polyphenols showed high cytotoxic activity in three cancer cell lines tested: cervical adenocarcinoma (HeLa), colon cancer (HCT116), and osteosarcoma (U2OS). The strongest inhibition of cell growth was observed in the HCT116 cell line. All cancer cells tested were more sensitive to treatment with polyphenols isolated from plants with added Si than those without added Si. The cytotoxic activity of the extracts on the healthy cell line RPE1 was similar to that on the cancer cell line HCT116 and U2OS.
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Kim, Woojung, Eun Sun Kim, Geeho Min, et al. "Two-photon probes for pH: Detection of human colon cancer using two-photon microscopy." Journal of Clinical Oncology 36, no. 4_suppl (2018): 607. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.607.
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607 Background: In cancer cells, lysosomal pH decreases along with a concomitant increase in lysosomal volume and cathepsin expression levels. Lysosomes also play crucial roles in cancer progression following their release into the extracellular space. Since cancer cells invade a tissue by secreting degradative enzymes, the extracellular pH of tumor tissues becomes acidic. However, to date, there has been no report on the use of multi-photon microscopy (MPM) probes to image human colon cancer tissues. Methods: We have developed multi-photon (MP) pH-sensitive probes (BH-2 and BHEt-1) that exhibit absorption and emission maxima at 370 and 466 nm, and TP absorption cross-section values of 51 and 61 GM (1 GM = 10−50 cm4 s/photon), respectively, at 750 nm and pH 3.0 in a universal buffer (0.1 M citric acid, 0.1 M KH2PO4, 0.1 M Na2B4O7, 0.1 M Tris, 0.1 M KCl)/1,4-dioxane (7/ 3) solution. Results: The TPM images of CCD-18co (a normal colon cell line) and HCT116 cells (a colon cancer cell line) labeled with BH-2 were too dim to be distinguished. When the same cells were labeled with BHEt-1, however, the MPM image of the HCT116 cells was much brighter than that of CCD-18co cells, and the relative proportion of the acidic vesicles (Pacid) of the former was 5-fold larger than that of latter. BHEt-1 could also differentiate HepG2 cells (a human liver cancer cell line) from LX-2 cells (a human hepatic stellate cell line) with a 6-fold larger P acid value. Human colon cancer tissues labeled with BHEt-1 showed similar results, demonstrating much brighter MPM images and 6-fold larger Pacid values compared to normal tissue. Conclusions: These results suggest the potential utility of BHEt-1 for molecular image analysis of colon cancer tissues using MPM.
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Kim, Sang-In, Shyambabu Chaurasiya, Anthony K. Park, et al. "Vitamin D as a Primer for Oncolytic Viral Therapy in Colon Cancer Models." International Journal of Molecular Sciences 21, no. 19 (2020): 7326. http://dx.doi.org/10.3390/ijms21197326.
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Oncolytic viroimmunotherapy is an exciting modality that can offer lasting anti-tumor immunity for aggressive malignancies like colon cancer. The impact of oncolytic viruses may be extended by combining them with agents to prime a tumor for viral susceptibility. This study investigates vitamin D analogue as an adjunct to oncolytic viral therapy for colon cancer. While vitamin D (VD) has historically been viewed as anti-viral, our in vitro investigations using human colon cancer cell lines showed that VD does not directly inhibit replication of recombinant chimeric poxvirus CF33. VD did restrict growth in HT29 but not HCT116 human colon cancer cells. In vivo investigations using HCT116 and HT29 xenograft models of colon cancer demonstrated that a VD analogue, calcipotriol, was additive with CF33-based viral therapy in VD-responsive HT29 but not in HCT116 tumors. Analyses of RNA-sequencing and gene expression data demonstrated a downregulation in the Jak-STAT signaling pathway with the addition of VD to viral therapy in HT29 models suggesting that the anti-inflammatory properties of VD may enhance the effects of viral therapy in some models. In conclusion, VD may prime oncolytic viral therapy in certain colon cancers.
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Kardan, Mostafa, Alireza Rafiei, Monireh Golpour, Mohammad Ali Ebrahimzadeh, Haleh Akhavan-Niaki, and Sadegh Fattahi. "Urtica dioica Extract Inhibits Cell Proliferation and Induces Apoptosis in HepG2 and HTC116 as Gastrointestinal Cancer Cell Lines." Anti-Cancer Agents in Medicinal Chemistry 20, no. 8 (2020): 963–69. http://dx.doi.org/10.2174/1871520620666200311095836.
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Background: Nowadays the use of plant-derived products has been extensively examined in the treatment of many types of gastrointestinal cancers such as hepatocarcinoma and colon cancer. Urtica dioica is a traditional herb that has many pharmacological effects and wildly used as a therapeutic agent in cancer. Herein, we have evaluated the effects of the different concentrations of Methanolic Extract of Urtica dioica (MEUD) on viability, death pattern, and expression of the apoptosis-related gene in normal Human Dermal Fibroblast (HDF), hepatocarcinoma cell lines (HepG2) and colon-cancer cell line (HCT116). Methods: A high-performance liquid chromatography method was developed to simultaneously separate 3 phenolic acids in MEUD. HepG2 and HCT116 cell lines as well as HDF normal cell line were cultured in suitable media. After 24 and 48h, in the cultured cell with different concentrations of MEUD, cells viability was assessed by MTT assay, and apoptosis was also evaluated at the cellular level by Annexin V/PI flow cytometry analyzing and AO/EB staining. BCL2 and BAX gene expressions were assessed by TaqMan real-time PCR assay. Results: MEUD showed antiproliferative effects on HepG2 and HTC116 cells after 48h with an IC50 value of about 410 and 420μg/ml, respectively (P < 0.001). Apoptotic cells were observed in HepG2 and HTC116 cells but not in HDF. Furthermore, the increased level of BAX/BCL-2 ratio was observed in HepG2 and HTC116 cells under the treatment of different concentrations of MEUD. Conclusions: The MEUD may influence hepatocarcinoma and colon-cancer cell lines at specific doses and change their proliferation rate by changing the expression of BAX and BCL2.
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Hussein, Ali N., Omar F. Abdul- Rasheed, Monther F. Mahdi, and Ayad M. R. Raauf. "The Evaluation of Antiproliferative Effect of Imatinib derivatives Against Breast and Colon Cell-Lines." International Journal of Pharmaceutical Quality Assurance 11, no. 01 (2013): 74–82. http://dx.doi.org/10.25258/ijpqa.11.1.22.
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Background: Cancer is considered as one of the major leading causes of death. Tyrosine kinase inhibitors are recognized for their potential antiproliferative effects. Materials and methods: In the previous study, the authors designed, synthesized, and characterized two imatinib derivatives. These derivatives were biologically evaluated with the utilization of MCF-7, HCT116, and MDCK cell lines. Results: In respect to the imatinib standard, compound 2b has superior activity against HCT116 cell line (IC50; 15.88 μg/mL against 18.52 μg/mL for imatinib) and an improved cytotoxic activity on MDCK cell line (IC50; 0.654 mg/mL against 0.272 mg/mL for imatinib). Conclusion: The two synthesized compounds showed biological activity against cancerous cell lines and improved cytotoxic activity against normal non-cancerous cell line with respect to the imatinib standard.
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El Newahie, Aliya, Yassin Nissan, Nasser Ismail, Dalal Abou El Ella, Sohair Khojah, and Khaled Abouzid. "Design and Synthesis of New Quinoxaline Derivatives as Anticancer Agents and Apoptotic Inducers." Molecules 24, no. 6 (2019): 1175. http://dx.doi.org/10.3390/molecules24061175.
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The quinoxaline scaffold is a promising platform for the discovery of active chemotherapeutic agents. Three series of quinoxaline derivatives were synthesized and biologically evaluated against three tumor cell lines (HCT116 human colon carcinoma, HepG2, liver hepatocellular carcinoma and MCF-7, human breast adenocarcinoma cell line), in addition to VEGFR-2 enzyme inhibition activity. Compounds VIId, VIIIa, VIIIc, VIIIe and XVa exhibited promising activity against the tested cell lines and weak activity against VEGFR-2. Compound VIIIc induced a significant disruption in the cell cycle profile and cell cycle arrest at the G2/M phase boundary. In further assays, the cytotoxic effect of the highly active compounds was determined using a normal Caucasian fibroblast-like fetal lung cell line (WI-38). Compound VIIIc could be considered as a lead compound that merits further optimization and development as an anti-cancer and an apoptotic inducing candidate against the HCT116 cell line.
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Lagal, Daniel J., Antonio M. Montes-Osuna, Alberto Ortiz-Olivencia, et al. "Tumoral Malignancy Decreases Coupled with Higher ROS and Lipid Peroxidation in HCT116 Colon Cancer Cells upon Loss of PRDX6." Antioxidants 13, no. 7 (2024): 881. http://dx.doi.org/10.3390/antiox13070881.
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Peroxiredoxin 6 (PRDX6) is an atypical member of the peroxiredoxin family that presents not only peroxidase but also phospholipase A2 and lysophosphatidylcholine acyl transferase activities able to act on lipid hydroperoxides of cell membranes. It has been associated with the proliferation and invasive capacity of different tumoral cells including colorectal cancer cells, although the effect of its removal in these cells has not been yet studied. Here, using CRISPR/Cas9 technology, we constructed an HCT116 colorectal cancer cell line knockout for PRDX6 to study whether the mechanisms described for other cancer cells in terms of proliferation, migration, and invasiveness also apply in this tumoral cell line. HCT116 cells lacking PRDX6 showed increased ROS and lipid peroxidation, a decrease in the antioxidant response regulator NRF2, mitochondrial dysfunction, and increased sensitivity to ferroptosis. All these alterations lead to a decrease in proliferation, migration, and invasiveness in these cells. Furthermore, the reduced migratory and invasive capacity of HCT116 cancer cells is consistent with the observed cadherin switch and decrease in pro-invasive proteins such as MMPs. Therefore, the mechanism behind the effects of loss of PRDX6 in HCT116 cells could differ from that in HepG2 cells which is coherent with the fact that the correlation of PRDX6 expression with patient survival is different in hepatocellular carcinomas. Nonetheless, our results point to this protein as a good therapeutic target also for colorectal cancer.
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SIM, EDMUND UI-HANG, SELVAMALAR MUTSAMY, and ZY-YING TEH. "EXPRESSION PATTERNS OF THE HUMAN RIBOSOMAL PROTEIN GENES eL14 AND uS19 IN COLON CANCER IS DEPENDENT ON THE TYPE AND STAGE OF THE CANCER CELL." Malaysian Applied Biology 49, no. 1 (2020): 31–39. http://dx.doi.org/10.55230/mabjournal.v49i1.1652.
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Although the association of some ribosomal protein genes with colorectal cancer is widely known, the detailed mechanisms and complete list of associated genes is lacking. More importantly, the behaviours of these genes in different types and stages of the cancer are poorly understood. Herein we report the study of two ribosomal protein genes in cell lines derived from different sites and stages of colon cancer. Specifically, we analysed the expression pattern of eL14 and uS19 in HCT116 and SW480 cell lines. These two genes, although associated with a wide variety of cancer types, are poorly or have not been studied in colorectal cancer. Semi-quantitative reverse transcription – polymerase chain reaction (RT-PCR) approach was used, together with Students’ t-test validation. We found a significantly (p < 0.05) differential eL14 and uS19 expression patterns between HCT116 and SW480 cell lines. Our findings suggest that eL14 and uS19 have higher activity in a poorly differentiated cell line derived from advanced (metastatic) stage (Duke’s Stage D) colorectal carcinoma tissues compared to the moderately differentiated cell line derived from a mid-stage (Duke’s Stage B) colorectal adenocarcinoma tumour. This will have important implications for both ribosomal protein genes as type and stage specific biomarkers for colon cancer
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Khaing, Ei Mon, Thanika Saenpunya, Pittawas Kerdklai, et al. "Combination Effects of Gambogic Acid on Imatinib Mesylate Cytotoxicity in Colon Cancer Cells." Key Engineering Materials 859 (August 2020): 27–33. http://dx.doi.org/10.4028/www.scientific.net/kem.859.27.
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Imatinib mesylate (IM) is a kinase inhibitor with inhibitory effect on colon cancer cell proliferation. However, some adverse effect of imatinib and drug resistance are challenges for maintenance the therapeutic effect with lowering the dose; thus, the combination with other substances was of interest. Gambogic acid (GA), a natural compound from gamboge, was revealed for inhibition of cell proliferation in many types of cancers. This research aimed to investigate the effect of GA on IM response in colorectal cancer cells, HT29 and HCT116. The 50% inhibitory concentration (IC50) of IM and GA was determined. Concentrations which lower than IC50 of each compound were combined and tested for the combination effects on HT29 and HCT116 cells. The results were analyzed using isobologram to assess the types of interaction. The combination index (CI) of the tests was calculated at the 3 different percentages of inhibition (IC50, IC60 and IC70). The finding indicated that IC50 and IC60 of the combination of 5 and 7 μM IM with 0.2-1.2 μM GA showed antagonism while IC70 showed additive effect in HT29 cell line. In HCT116 cell line, IC50 of 10 μM IM with 0.1-0.8 μM GA showed antagonism while IC60 and IC70 expressed additive effect. For the studies with IC50 and IC60 of 12 μM IM with 0.1-0.8 μM GA showed antagonistic result while IC70 showed additive effect. The result indicated that, at the lower IC studied, the CI obtained from the experiments indicated the inhibitory effects, while the higher IC, the results showed the changing trend from antagonistic to additive and synergistic effects of GA on IM.
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BARUSRUX, Sahapat, Natthida WEERAPREEYAKUL, Preeyaporn Plaimee PHIBOONCHAIYANAN, Munthipha KHAMPHIO, Waraporn TANTHANUCH та Kanjana THUMMANU. "Anticancer Activity of Lindernia crustacea (L.) F. Muell. var. Crustacean on Human HCT116 Colon Cancer Cell via Cellular Lipid and β-sheet Protein Accumulation". Walailak Journal of Science and Technology (WJST) 17, № 11 (2020): 1211–20. http://dx.doi.org/10.48048/wjst.2020.10718.
Texte intégralRésumé :
Lindernia crustacea (L.) F. Muell. var. crustacean or “Ya Kap Hoi: YKH”, which is an edible vegetable, is commonly seen in Thailand. This study investigated its anticancer properties with high antioxidant activity by reducing power activity, excluding alkylation activity. It explored YKH extract induction of anticancer activity through biomolecular changes in the HCT116 human colon cancer cell line. The ethanolic extract stock solution and water extract stock solution were prepared. NR assay was used for cancer cell cytotoxic testing and Fourier transform infrared (FTIR) microspectroscopy was used for biomolecular changes study on lipid, protein and nucleic acid/DNA. The apoptosis induction by the extracts was detected by using Annexin V-FITC and DAPI staining. The compounds in the YKH ethanolic extract was performed by using GC-MS analysis. As a result, YKH ethanolic extract caused HCT116 colon cancer cell death in the dose dependent manner after 24 h exposure, and the 50 % cell death (IC50 concentration) was 195.4 ± 12 μg/mL. Cellular biochemical changes observed from FTIR data showed that YKH ethanolic extract treated HCT116 colon cancer cell. There is an increase in lipid content and a reduction in intensity of nucleic acid/DNA, a-helix protein structure at 1,656 cm-1 was reduced and peak position of b-sheet structure (1,637 cm-1) was shifted to lower frequency. From the analysis results, YKH ethanolic extract seems to exert anti-colon cancer effect by changing cellular biomolecular structure of lipids and β-sheet protein accumulation, supporting apoptotic induction. The compounds in the YKH ethanolic extract mainly yielded fatty acids,which may be useful as potential compounds.
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Ahmad, Nor Ezleen Qistina, Amirah Alhusna Mohd Yusoff, Nur Fariesha Md Hashim, Nurul Akmaryanti Abdullah, and Noraina Muhamad Zakuan. "Dimethyloxalylglycine (DMOG) Induced Hypoxia Promoted Migratory and Invasive Properties of HCT116 Colon Cancer Cell Line." Sains Malaysiana 53, no. 6 (2024): 1333–41. http://dx.doi.org/10.17576/jsm-2024-5306-09.
Texte intégralRésumé :
Hypoxia, a condition characterised by low oxygen levels, leads to increased production of a protein called hypoxia-inducible factor-1 alpha (HIF-1α) in cancer cells. This protein is involved in driving processes such as vascularization, cytoskeletal reorganisation, and epithelial-to-mesenchymal transformation (EMT), which contribute to metastasis. Previous studies used hypoxic workstations, chambers, and incubators to evaluate the effects of hypoxia on colon cancer cell lines. In a cell culture model, hypoxic conditions can also be induced using dimethyloxalylglycine (DMOG) as the hypoxia-mimicking agent. This study aims to investigate the effects of DMOG-induced hypoxia on colon cancer metastasis, focusing on cell migration and invasion. HCT116 cells were subjected to hypoxic conditions by treating them with DMOG, and the expression of HIF-1α proteins was measured at various time points, followed by wound healing and invasion assays. It was found that HIF-1α protein expression increases after 6 h of DMOG induction and persists for 24 h. At 6 and 24 h, a significantly higher percentage of hypoxic cells migrated compared to normoxic cells. The invasion assay demonstrated that hypoxic cells were more invasive than normoxic cells within 24 h. Thus, the increase in migration and invasion of cells is comparable to the increase in HIF-1α expression at 6 and 24 h. These findings suggest that DMOG induces HIF-1α expression in colon cancer cells, leading to enhanced cell migration and invasiveness. The established model can be further utilised in gene knockdown or drug treatment studies to evaluate the effects of hypoxia on cancer cells.
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Wu, Yajiao, Xiaoying Chen, Wenqiang Bao, et al. "Effect of Humantenine on mRNA m6A Modification and Expression in Human Colon Cancer Cell Line HCT116." Genes 13, no. 5 (2022): 781. http://dx.doi.org/10.3390/genes13050781.
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Humantenine, an alkaloid isolated from the medicinal herb Gelsemium elegans (Gardner & Chapm.) Benth., has been reported to induce intestinal irritation, but the underlying toxicological mechanisms remain unclear. The object of the present study was to investigate the RNA N6-methyladenosine (m6A) modification and distinct mRNA transcriptome profiles in humantenine-treated HCT116 human colon cancer cells. High-throughput MeRIP-seq and mRNA-seq were performed, and bioinformatic analysis was performed to reveal the role of abnormal RNA m6A modification and mRNA expression in humantenine-induced intestinal cell toxicity. After humantenine treatment of HCT116 cells, 1401 genes were in the overlap of differentially m6A-modified mRNA and differentially expressed mRNA. The Kyoto Encyclopedia of Genes and Genomes and Gene Ontology annotation terms for actin cytoskeleton, tight junctions, and adherens junctions were enriched. A total of 11 kinds of RNA m6A methylation regulators were differentially expressed. The m6A methylation levels of target genes were disordered in the humantenine group. In conclusion, this study suggested that the HCT116 cell injury induced by humantenine was associated with the abnormal mRNA expression of m6A regulators, as well as disordered m6A methylation levels of target genes.
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Oliveira, Susana Mendonça, Patrícia Dias Carvalho, André Serra-Roma, et al. "Fibroblasts Promote Resistance to KRAS Silencing in Colorectal Cancer Cells." Cancers 16, no. 14 (2024): 2595. http://dx.doi.org/10.3390/cancers16142595.
Texte intégralRésumé :
Colorectal cancer (CRC) responses to KRAS-targeted inhibition have been limited due to low response rates, the mechanisms of which remain unknown. Herein, we explored the cancer-associated fibroblasts (CAFs) secretome as a mediator of resistance to KRAS silencing. CRC cell lines HCT15, HCT116, and SW480 were cultured either in recommended media or in conditioned media from a normal colon fibroblast cell line (CCD-18Co) activated with rhTGF-β1 to induce a CAF-like phenotype. The expression of membrane stem cell markers was analyzed by flow cytometry. Stem cell potential was evaluated by a sphere formation assay. RNAseq was performed in KRAS-silenced HCT116 colonospheres treated with either control media or conditioned media from CAFs. Our results demonstrated that KRAS-silencing up-regulated CD24 and down-regulated CD49f and CD104 in the three cell lines, leading to a reduction in sphere-forming efficiency. However, CAF-secreted factors restored stem cell marker expression and increased stemness. RNA sequencing showed that CAF-secreted factors up-regulated genes associated with pro-tumorigenic pathways in KRAS-silenced cells, including KRAS, TGFβ, NOTCH, WNT, MYC, cell cycle progression and exit from quiescence, epithelial-mesenchymal transition, and immune regulation. Overall, our results suggest that resistance to KRAS-targeted inhibition might derive not only from cell-intrinsic causes but also from external elements, such as fibroblast-secreted factors.
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Garcia, Joseph A., Rui Chen, Min Xu, et al. "Acss2/HIF-2 signaling facilitates colon cancer growth and metastasis." PLOS ONE 18, no. 3 (2023): e0282223. http://dx.doi.org/10.1371/journal.pone.0282223.
Texte intégralRésumé :
The microenvironment of solid tumors is characterized by oxygen and glucose deprivation. Acss2/HIF-2 signaling coordinates essential genetic regulators including acetate-dependent acetyl CoA synthetase 2 (Acss2), Creb binding protein (Cbp), Sirtuin 1 (Sirt1), and Hypoxia Inducible Factor 2α (HIF-2α). We previously shown in mice that exogenous acetate augments growth and metastasis of flank tumors derived from fibrosarcoma-derived HT1080 cells in an Acss2/HIF-2 dependent manner. Colonic epithelial cells are exposed to the highest acetate levels in the body. We reasoned that colon cancer cells, like fibrosarcoma cells, may respond to acetate in a pro-growth manner. In this study, we examine the role of Acss2/HIF-2 signaling in colon cancer. We find that Acss2/HIF-2 signaling is activated by oxygen or glucose deprivation in two human colon cancer-derived cell lines, HCT116 and HT29, and is crucial for colony formation, migration, and invasion in cell culture studies. Flank tumors derived from HCT116 and HT29 cells exhibit augmented growth in mice when supplemented with exogenous acetate in an Acss2/HIF-2 dependent manner. Finally, Acss2 in human colon cancer samples is most frequently localized in the nucleus, consistent with it having a signaling role. Targeted inhibition of Acss2/HIF-2 signaling may have synergistic effects for some colon cancer patients.
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Neupane, Rabin, Saloni Malla, Mariam Sami Abou-Dahech, et al. "Antiproliferative Efficacy of N-(3-chloro-4-fluorophenyl)-6,7-dimethoxyquinazolin-4-amine, DW-8, in Colon Cancer Cells Is Mediated by Intrinsic Apoptosis." Molecules 26, no. 15 (2021): 4417. http://dx.doi.org/10.3390/molecules26154417.
Texte intégralRésumé :
A novel series of 4-anilinoquinazoline analogues, DW (1–10), were evaluated for anticancer efficacy in human breast cancer (BT-20) and human colorectal cancer (CRC) cell lines (HCT116, HT29, and SW620). The compound, DW-8, had the highest anticancer efficacy and selectivity in the colorectal cancer cell lines, HCT116, HT29, and SW620, with IC50 values of 8.50 ± 2.53 µM, 5.80 ± 0.92 µM, and 6.15 ± 0.37 µM, respectively, compared to the non-cancerous colon cell line, CRL1459, with an IC50 of 14.05 ± 0.37 µM. The selectivity index of DW-8 was >2-fold in colon cancer cells incubated with vehicle. We further determined the mechanisms of cell death induced by DW-8 in SW620 CRC cancer cells. DW-8 (10 and 30 µM) induced apoptosis by (1) producing cell cycle arrest at the G2 phase; (2) activating the intrinsic apoptotic pathway, as indicated by the activation of caspase-9 and the executioner caspases-3 and 7; (3) nuclear fragmentation and (4) increasing the levels of reactive oxygen species (ROS). Overall, our results suggest that DW-8 may represent a suitable lead for developing novel compounds to treat CRC.
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Wongkaewkhiaw, Saharut, Amaraporn Wongrakpanich, Sucheewin Krobthong, Witchuda Saengsawang, Arthit Chairoungdua, and Nittaya Boonmuen. "Induction of apoptosis in human colorectal cancer cells by nanovesicles from fingerroot (Boesenbergia rotunda (L.) Mansf.)." PLOS ONE 17, no. 4 (2022): e0266044. http://dx.doi.org/10.1371/journal.pone.0266044.
Texte intégralRésumé :
Colorectal cancer is the leading cause of cancer-related deaths worldwide, warranting the urgent need for a new treatment option. Plant-derived nanovesicles containing bioactive compounds represent new therapeutic avenues due to their unique characteristics as natural nanocarriers for bioactive molecules with therapeutic effects. Recent evidence has revealed potential anticancer activity of bioactive compounds from Boesenbergia rotunda (L.) Mansf. (fingerroot). However, the effect and the underlying mechanisms of fingerroot-derived nanovesicles (FDNVs) against colorectal cancer are still unknown. We isolated the nanovesicles from fingerroot and demonstrated their anticancer activity against two colorectal cancer cell lines, HT-29 and HCT116. The IC50 values were 63.9 ± 2.4, 57.8 ± 4.1, 47.8 ± 7.6 μg/ml for HT-29 cells and 57.7 ± 6.6, 47.2 ± 5.2, 34 ± 2.9 μg/ml for HCT116 cells at 24, 48, and 72 h, respectively. Interestingly, FDNVs were not toxic to a normal colon epithelial cell line, CCD 841 CoN. FDNVs exhibited selective uptake by the colorectal cancer cell lines but not the normal colon epithelial cell line. Moreover, dose- and time-dependent FDNV-induced apoptosis was only observed in the colorectal cancer cell lines. In addition, reactive oxygen species levels were substantially increased in colorectal cancer cells, but total glutathione decreased after treatment with FDNVs. Our results show that FDNVs exhibited selective anticancer activity in colorectal cancer cell lines via the disruption of intracellular redox homeostasis and induction of apoptosis, suggesting the utility of FDNVs as a novel intervention for colorectal cancer patients.
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Wang, Xiaoqi, Xincheng Lu, Guangjin Zhou, Hua Lou, and Guangbin Luo. "RECQL5 is an important determinant for camptothecin tolerance in human colorectal cancer cells." Bioscience Reports 31, no. 5 (2011): 363–69. http://dx.doi.org/10.1042/bsr20100108.
Texte intégralRésumé :
CPTs (camptothecins) are an important class of effective anticancer agents that target type I topoisomerase in humans. Irinotecan and topotecan are currently used to treat various types of cancers and many CPT derivatives are being developed. However, these drugs are only effective in a small percentage of each type of cancer and the molecular underpinning for this individualized response to the drug has remained elusive. Thus, identification of the main determinants for cell survival in response to this unique class of drug should help to improve their clinical applications. In the present study, we examined whether RECQL5 constitutes an important determinant of CPT resistance in colon cancer cells. Specifically, RECQL5-deficient derivatives of both DDL1 and HCT116 cells, two colorectal cancer cell lines were generated by adenovirus-based somatic gene-targeting experiments and the CPT sensitivity between the RECQL5-proficient parental lines and their corresponding RECQL5-deficient derivatives were examined. We found that deletion of RECQL5 from DDL1 and HCT116 cells both resulted in a significant enhancement in CPT sensitivity under in vitro culture conditions. More importantly, xenograft tumours derived from RECQL5-deficient HCT116 cells, but not those from the parental line, could be cured by a CPT-based therapy in nude mice. Thus, the present study has identified RECQL5 as a major determinant for CPT resistance in colorectal cancer cells and a potential candidate as a biomarker for irinotecan-based treatment for colon cancer.
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Ljujic, M., S. Mijatovic, M. Z. Bulatovic, et al. "ALPHA-1 antitrypsin affects U0126-induced cytotoxicity in colon cancer cell line (HCT116)." Molecular Biology 50, no. 1 (2016): 153–56. http://dx.doi.org/10.1134/s002689331601012x.
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Rao, Poorima BN, and Farah Deeba. "Expressions of biomarkers in MCF7 Breast and Colon Cancer Cell Lines." Journal of Drug Delivery and Therapeutics 10, no. 2 (2020): 107–14. http://dx.doi.org/10.22270/jddt.v9i4-s.3993.
Texte intégralRésumé :
Cancer is one of the leading causes of death which accounts for 13% of total deaths, worldwide. Colorectal and Breast cancer fall under main categories according to World Health Organisation (WHO) cancer facts sheet 1. The need to understand the expression of clinical biomarkers in breast cancer and colon cancer is necessary for diagnosis and therapeutic response. In this article, the expressions of histone H1 and TP53 biomarkers were established for four different colon cancer cell lines and compared with the expressions of MCF7 cell line. The results show varied expression of Histone H1 along with TP53 markers among the cell lines. The results suggest that the linker Histone H1 has shown nuclear localization in HCT 116p53 wt (wild type) cancer cell line whereas it has shown cytoplasmic distribution in the respective null type cell line with intense expression. The result also suggests that a localized distribution in HRA19 cells and a diffused distribution in SNU-C2B cell line. These established results were compared with the expression of the biomarkers in MCF7 in order to get a better understanding.
 Keywords: Tumour Proteins, p53, H1, MCF-7 cell, HCT116, HRA19.
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Ko, Hyun Min, Wona Jee, Do-il Park, Kwan-Il Kim, Ji Hoon Jung, and Hyeung-Jin Jang. "The Antitumor Effect of Timosaponin A3 through c-Myc Inhibition in Colorectal Cancer Cells and Combined Treatment Effect with 5-FU or Doxorubicin." International Journal of Molecular Sciences 23, no. 19 (2022): 11900. http://dx.doi.org/10.3390/ijms231911900.
Texte intégralRésumé :
Timosaponin A3 (TA3), extracted from the rhizome of Anemarrhenaasphodeloides Bunge, has been reported to affect various diseases, such as cancer, Alzheimer’s disease, and allergies. However, the underlying molecular mechanisms and impacts are largely unknown. In the present study, we hypothesized that TA3 induces apoptosis through the inhibition of c-Myc expression via CNOT2 or MID1IP1 in HCT116. An MTT assay and colony formation assay were used to measure cell viability and proliferation. The protein expression of apoptotic markers and oncogenes was measured using immunoblotting and immunofluorescence assays. The interaction between MID1IP1 and c-Myc was confirmed by performing an immunoprecipitation assay. TA3 markedly inhibited colon cancer cell proliferation. Consistently, TA3 regulated the apoptotic proteins pro-PARP and caspase 3. TA3 inhibited the half-life of c-Myc and suppressed its expression in response to serum stimulation. In addition, TA3 enhanced the apoptotic effects of doxorubicin and 5-FU in colon cancer cells. Altogether, our results reveal a mechanism by which TA3 induces apoptosis through inhibiting c-Myc expression via CNOT2 or MID1IP1 in HCT116, which may help in the development of new therapies for colon cancer based on TA3 in the future.
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Lee, Woo, Yoo, Cho, and Kim. "Differential Mechanism of ATP Production Occurs in Response to Succinylacetone in Colon Cancer Cells." Molecules 24, no. 19 (2019): 3575. http://dx.doi.org/10.3390/molecules24193575.
Texte intégralRésumé :
Our aim was to verify the potential ability of succinylacetone (SA) to inhibit mitochondrial function, thereby suppressing cancer cell proliferation. SA treatment caused apoptosis in HCT116 and HT29 cells, but not in SW480 cells, with mitochondria playing a key role. We checked for dysfunctional mitochondria after SA treatment. Mitochondria of HT29 cells were swollen, indicating damage, whereas in HCT116 cells, several mitochondria had a diminished size. Damaged mitochondria decreased ATP production and induced reactive oxygen species (ROS) in the cells. To understand SA-induced reduction in ATP production, we investigated the electron transfer chains (ETC) and pyruvate dehydrogenase kinase (PDK) activity, which prevents the transfer of acetyl-CoA to the TCA (tricarboxylic acid) cycle by inhibiting PDH (pyruvate dehydrogenase) activity. In each cell line, the inhibitory mechanism of ATP by SA was different. The activity of complex III consisting of the mitochondrial ETCs in HT29 cells was decreased. In contrast, PDH activity in HCT116 cells was reduced. Nicotinamide nucleotide transhydrogenase (NNT)-removing reactive oxygen species (ROS) was upregulated in HT29 cells, but not in HCT116 cells, indicating that in HT29 cells, a defense mechanism was activated against ROS. Collectively, our study showed a differential mechanism occurs in response to SA in colon cancer cells.
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Thanuja, B., R. Parimalavalli, S. Vijayanand, et al. "Anticancer and Cytotoxicity Activity of Native and Modified Black Rice Flour on Colon Cancer Cell Lines." Evidence-Based Complementary and Alternative Medicine 2022 (February 21, 2022): 1–9. http://dx.doi.org/10.1155/2022/8575026.
Texte intégralRésumé :
This study is intended to evaluate the cytotoxicity of native and dual-modified black rice flour against the colon cancer cell line (HCT116) and mouse embryo cell line (3T3-L1) by using the MTT assay. The modification techniques applied to prepare rice flour samples were enzymatic modification and heat moisture treatment. In this study, the IC50 of native black rice flour and modified black rice flour was 255.78 µg/mL and 340.85 µg/mL, respectively. The result confirms that the native black rice flour has significant cytotoxic and anticancer potential against human colon cancer cells. In addition, the IC50 of native black rice flour and modified black rice flour on the 3T3-L1 cell line was found to be 345.96 µg/mL and 1106.94 µg/mL, respectively. The results showed that the native black rice flour had weak cytotoxicity, and modified black rice flour was nontoxic in both the cell lines. The active component of phytochemicals present in black rice flour has a potential role in preventing colon cancer.
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Su, Meng-Qi, Yi-Ran Zhou, Cheng-Qin Li, et al. "Zedoary Turmeric Oil Induces Senescence and Apoptosis in Human Colon Cancer HCT116 Cells." Natural Product Communications 13, no. 7 (2018): 1934578X1801300. http://dx.doi.org/10.1177/1934578x1801300731.
Texte intégralRésumé :
Zedoary turmeric oil (ZTO) is a volatile oil that is extracted from the dry rhizome of Curcuma zedoaria with a variety of biological activities, including anti-tumor activity. However, there is a lack of knowledge about the effect and mechanism of ZTO in human colon cancer cells. The aim of this study was to examine the potential efficacy of ZTO against human colon cancer cells (HCT116) and to uncover the molecular mechanisms of its anti-tumor effects. The anti-proliferative activity of ZTO was determined by the MTT assay, cell counts and colony formation assay. Senescent cells were detected using SA-β-Gal staining, while apoptosis and the CD44+ subpopulation were evaluated by flow cytometry. The expression levels of senescence- and apoptosis-related proteins were examined using western blotting. The results showed that treatment with ZTO significantly inhibited the growth of HCT116 cells and caused senescence and apoptosis in a dose- and time-dependent manner. Western blotting revealed that ZTO significantly increased the expression of senescence- and apoptosis-related proteins p16, p21, and p53 and the phosphorylation of ERK. Moreover, ZTO treatment reduced the cancer stem-like CD44 positive cell population. These findings suggest that ZTO inhibits human colon cancer cells by inducing senescence and apoptosis.
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Tao, Han-chuan, Cheng Wang, Ning Ma, Xun Zhu, and Xiao-jun Zhou. "Recurrent Superenhancer of the Oncogene POU5F1B in Colorectal Cancers." BioMed Research International 2021 (December 11, 2021): 1–11. http://dx.doi.org/10.1155/2021/5405060.
Texte intégralRésumé :
Superenhancer usages in single cancer form such as colorectal cancer (CRC) may provide novel efficient targeting candidates. It is unclear whether CRC contains recurrent superenhancers that confer a predisposition to malignancy. We investigated the superenhancer profile of CRC cell line HCT116 and compared it to that of a healthy sigmoid colon. We found that HCT116 had lost most of the normal colon superenhancer activities but gained a new set of tumor-favoring superenhancers that facilitate tumor proliferation, growth signalling, and hypoxia resistance. Inhibiting the superenhancers by JQ-1 treatment had significantly decreased the colony formation capability of HCT116. Then, by comparing the superenhancer genes and robust CRC upregulated genes, we identified a superenhancer associated with a common CRC upregulated oncogene, POU5f1B. POU5f1B overexpression is related to the worse outcome in CRCs. Via performing ChIP-PCR in 35 clinical samples and investigating CRC anti-H3K27ac ChiP-seq public dataset consisting of 36 samples, we further identified that the superenhancer of oncogene POU5F1B is recurrently activated in CRCs, taking 62 and 72 per cent, respectively. Moreover, JQ-1 treatment successfully inhibited the POU5F1B expression in 5 out of 6 POU5F1B superenhancer-positive samples. Therefore, we concluded that the superenhancer activation of POU5F1B contributes partially to its high expression in CRCs, in addition to the well-known gene amplification aetiology.
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Godesi, Sreenivasulu, Hossam Nada, Joohan Lee, et al. "Integration of Hybridization Strategies in Pyridine–Urea Scaffolds for Novel Anticancer Agents: Design, Synthesis, and Mechanistic Insights." Molecules 28, no. 13 (2023): 4952. http://dx.doi.org/10.3390/molecules28134952.
Texte intégralRésumé :
Annually, millions of new cancer cases are reported, leading to millions of deaths worldwide. Among the newly reported cases, breast and colon cancers prevail as the most frequently detected variations. To effectively counteract this rapid increase, the development of innovative therapies is crucial. Small molecules possessing pyridine and urea moieties have been reported in many of the currently available anticancer agents, especially VEGFR2 inhibitors. With this in mind, a rational design approach was employed to create hybrid small molecules combining urea and pyridine. These synthesized compounds underwent in vitro testing against breast and colon cancer cell lines, revealing potent submicromolar anticancer activity. Compound 8a, specifically, exhibited an impressive GI50 value of 0.06 μM against the MCF7 cancer cell line, while compound 8h displayed the highest cytotoxic activity against the HCT116 cell line, with a GI50 of 0.33 ± 0.042 μM. Notably, compounds 8a, 8h, and 8i demonstrated excellent safety profiles when tested on normal cells. Molecular docking, dynamic studies, and free energy calculations were employed to validate the affinity of these compounds as VEGFR2 inhibitors.
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Al-Wahaibi, Lamya H., Hanaa M. Abu-Melha, and Diaa A. Ibrahim. "Synthesis of Novel 1,2,4-Triazolyl Coumarin Derivatives as Potential Anticancer Agents." Journal of Chemistry 2018 (October 14, 2018): 1–8. http://dx.doi.org/10.1155/2018/5201374.
Texte intégralRésumé :
A series of novel coumarin derivatives carrying 1,2,4-triazole or 1,2,4-triazolo[3,4-b][1,3,4]thiadiazole moieties were prepared and evaluated in vitro as anticancer in the human colon cancer (HCT116) cell line. The derivatives 4c and 8c exhibited marked anticancer activity with IC50 values 4.363 and 2.656 µM, respectively. The molecular docking studies suggested possible interaction with tyrosine kinases (CDK2).
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Negm, Amr, Azza Sedky, and Hany Elsawy. "Capric Acid Behaves Agonistic Effect on Calcitriol to Control Inflammatory Mediators in Colon Cancer Cells." Molecules 27, no. 19 (2022): 6624. http://dx.doi.org/10.3390/molecules27196624.
Texte intégralRésumé :
Inflammation prompts cancer development and promotes all stages of tumorigenesis. Calcitriol is a nutraceutical essential regulator for host health benefits. However, the influence of calcitriol on inflammatory mediators involved in cancer cells is not clear. This study aimed to assess the sensitivity of calcitriol alone and combined with capric acid, and identify the possible influence of calcitriol on inflammatory mediators. The colorectal cancer cell line (HCT116) was induced by LPS/TNF-α and the inflammation and metastatic mediators (IL-1β, IL-6, IL-17) were quantified in calcitriol and capric acid supplemented colon cancer cells. The mRNA and protein expression of MMP-2, NF-κB and COX-2 were quantified. The significant reduction in MMP-2 expression was confirmed at combination treatment by zymogram analysis. Our findings demonstrated the anti-inflammatory and anti-metastatic potentials of capric acid and calcitriol in individual exposure in a combination of human colon cancer cell lines (HCT116). These abilities may be due to the inhibition of COX-2 mediators and NF-κB transcription factor and reciprocally regulated MMP-2 and MMP-9 signaling pathways. These findings elucidate the activation of COX-2 and NF-κB via disruption of the cellular outer matrix could be considered a novel molecular target suitable for colorectal cancer therapy. This study confirmed that capric acid activates calcitriol sensitization in colon cancer cells and could be used as a successful supplement for intestinal diseases and colon aberrations.
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Samir, Nermin, Riham F. George, Eman Z. Elrazaz, et al. "Synthesis of some tropane-based compounds targeting colon cancer." Future Medicinal Chemistry 12, no. 23 (2020): 2123–40. http://dx.doi.org/10.4155/fmc-2020-0097.
Texte intégralRésumé :
Background: In continuation of a previous work concerned with the anticancer activity of some 8-alkyl-2,4-bisarylidene-8-nortropan-3-ones, this work focuses on further modification to the tropane/pyran fused skeleton aiming to obtain improved anticancer activity. Methodology: Reaction of 8-alkyl-2,4-bisarylidene-8-nortropan-3-ones 1–21 with malononitrile under basic conditions afforded tropane/pyran hybrids 22–40 and tropane/pyridine hybrids 41, 42. X-ray crystallography for compounds 22 and 41 as representative examples confirmed their structures. They were tested for their anticancer activity in the HCT116 cell line. Results: Compounds 26 and 33 were the most active compounds with IC50 values of 3.39 and 0.01 μM against HCT116. Moreover, they revealed cyclin-dependent kinase-2 (CDK2) inhibition with IC50 = 104.91 and 49.13 nM, respectively. Furthermore, molecular docking of compounds 26 and 33 in the active site of CDK2 confirmed the obtained results. Conclusion: Tropane/pyran scaffold can be considered as a promising core for anticancer agents acting as CDK2 inhibitors.
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Ali, Zainab M., Haitham Mahmood Kadhim, Omeed M. Hassan, Ammar Kubba, Zeena A. Hussein, and Hayder B. Sahib. "Antiangiogenic activity of 5-bromoindole carbothioamide derivative in ex vivo, in vivo, and in vitro experimental study." Pharmacia 71 (August 28, 2024): 1–9. https://doi.org/10.3897/pharmacia.71.e128589.
Texte intégralRésumé :
The study aimed to investigate the antiangiogenic, antioxidant, and cytotoxicity activity of a carbothioamide indole derivative. The 2-NPHC activity was evaluated using the <i>ex vivo</i> rat aorta ring assay, the <i>in vivo</i> chick chorioallantois membrane assay, the DPPH assay for scavenging activity, and the expression of the <i>VEGF</i> gene in colon cancer cell line (HCT116). The 2-NPHC had significant antiangiogenic activity in a dose-dependent manner in the rat aorta assay. 2-NPHC managed to reduce the DPPH free radical in a concentration-dependent, 2-NPHC had low to non-toxic effects on the HUVEC cell line, with an IC50 value of 711.7 μg/ml. The <i>VEGF</i> gene expression in the HCT116 cell line reduced the target gene expression compared to control cells. In conclusion, 2-NPHC exhibited significant inhibition of the angiogenesis process, either directly by inhibiting the release or activity of VEGF or indirectly through its antioxidant properties.
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Szaryńska, Magdalena, Agata Olejniczak-Kęder, Kamila Podpłońska, Adam Prahl, and Emilia Iłowska. "Bradykinin and Neurotensin Analogues as Potential Compounds in Colon Cancer Therapy." International Journal of Molecular Sciences 24, no. 11 (2023): 9644. http://dx.doi.org/10.3390/ijms24119644.
Texte intégralRésumé :
Colorectal cancer (CRC) is one of the most lethal malignancies worldwide, so the attempts to find novel therapeutic approaches are necessary. The aim of our study was to analyze how chemical modifications influence physical, chemical, and biological properties of the two peptides, namely, bradykinin (BK) and neurotensin (NT). For this purpose, we used fourteen modified peptides, and their anti-cancers features were analyzed on the HCT116 CRC cell line. Our results confirmed that the spherical mode of a CRC cell line culture better reflects the natural tumour microenvironment. We observed that the size of the colonospheres was markedly reduced following treatment with some BK and NT analogues. The proportion of CD133+ cancer stem cells (CSCs) in colonospheres decreased following incubation with the aforementioned peptides. In our research, we found two groups of these peptides. The first group influenced all the analyzed cellular features, while the second seemed to include the most promising peptides that lowered the count of CD133+ CSCs with parallel substantial reduction in CRC cells viability. These analogues need further analysis to uncover their overall anti-cancer potential.
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Lewkowski, Jarosław, Maria Rodriguez Moya, Anna Wrona-Piotrowicz, Janusz Zakrzewski, Renata Kontek, and Gabriela Gajek. "Synthesis, fluorescence properties and the promising cytotoxicity of pyrene–derived aminophosphonates." Beilstein Journal of Organic Chemistry 12 (June 16, 2016): 1229–35. http://dx.doi.org/10.3762/bjoc.12.117.
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A large series of variously substituted amino(pyren-1-yl)methylphosphonic acid derivatives was synthesized using a modified aza-Pudovik reaction in 20–97% yields. The fluorescence properties of the obtained compounds were investigated revealing that N-alkylamino(pyren-1-yl)methylphosphonic derivatives are stronger emissive compounds than the corresponding N-aryl derivatives. N-Benzylamino(pyren-1-yl)methylphosphonic acid displayed strong fluorescence (ΦF = 0.68) in phosphate-buffered saline (PBS). The influence of a series of derivatives on two colon cancer cell lines HT29 and HCT116 was also investigated. The most promising results were obtained for N-(4-methoxyphenyl)amino(pyren-1-yl)methylphosphonate, which was found to be cytotoxic for the HCT116 cancer cell line (IC50 = 20.8 μM), simultaneously showing weak toxicity towards normal lymphocytes (IC50 = 230.8 µM).
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Almansour, Abdulrahman I., Raju Suresh Kumar, Natarajan Arumugam, et al. "D-Ring-Modified Analogues of Luotonin A with Reduced Planarity: Design, Synthesis, and Evaluation of Their Topoisomerase Inhibition-Associated Cytotoxicity." BioMed Research International 2019 (November 13, 2019): 1–12. http://dx.doi.org/10.1155/2019/2514524.
Texte intégralRésumé :
A- and D-ring-modified luotonin-inspired heterocycles have been synthesized and were evaluated for their activity against the viability of four cancer cell lines in vitro, namely, MCF7, HCT116, JURKAT, and NCI-H460. The analysis of results indicated that two of the synthesized derivatives displayed good inhibition against the growth of the human colon cancer HCT116 cell line, with potencies lower than but in the same order of magnitude as camptothecin (CPT). These two luotonin analogues also showed an activity similar to that of the highly potent alkaloid CPT as inhibitors of topoisomerase I and also inhibited topoisomerase II. These results show that complete planarity is not a strict requirement for topoisomerase inhibition by luotonin-related compounds, paving the way to the design of analogues with improved solubility.
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Cai, Peng-Peng. "Effect of arsenic trioxide on growth and cell cycle progression in colon cancer cell line HCT116." World Chinese Journal of Digestology 22, no. 4 (2014): 563. http://dx.doi.org/10.11569/wcjd.v22.i4.563.
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Peng, Kui-Yuan, та Tz-Chong Chou. "Osthole Exerts Inhibitory Effects on Hypoxic Colon Cancer Cells via EIF2α Phosphorylation-mediated Apoptosis and Regulation of HIF-1α". American Journal of Chinese Medicine 50, № 02 (2022): 621–37. http://dx.doi.org/10.1142/s0192415x22500240.
Texte intégralRésumé :
Hypoxic microenvironment and dysregulated endoplasmic reticulum stress/unfolded protein response (UPR) system are considered important factors that promote cancer progression. Although osthole extracted from Cnidium monnieri(Fructus Cnidii) has been confirmed to exhibit an anticancer activity in various cancers, the effects of osthole in hypoxic colon cancer cells have not been explored. Therefore, the aim of this study was to examine whether osthole has an inhibitory effect on hypoxic colon cancer HCT116 cells and further investigate the underlying molecular mechanisms. Treatment with osthole significantly attenuated the cell viability, proliferation, and migration in hypoxic HCT116 cells. Osthole also activated UPR signaling such as phospho-eukaryotic initiation factor 2 alpha (EIF2[Formula: see text]/ATF4/CHOP/DR5 cascade accompanied by upregulation of pro-apoptotic proteins. Moreover, the tubule-like formation of human umbilical vein endothelial cells, the secretion of vascular endothelial growth factor A, and the expression and activity of hypoxia-inducible factor-1[Formula: see text] (HIF-1[Formula: see text] in hypoxic HCT116 cells were markedly suppressed by osthole. However, suppressing EIF2[Formula: see text] phosphorylation with salubrinal or ISRIB markedly reversed the effects of osthole on the expressions of pro-apoptotic proteins and HIF-1[Formula: see text]. Co-treatment of hypoxic HCT116 cells with osthole greatly increased the sensitivity to cisplatin and the expressions of phospho-EIF2[Formula: see text] and cleaved caspase 3. Collectively, the inhibitory effect of osthole in hypoxic HCT116 cells may be associated with EIF2[Formula: see text] phosphorylation-mediated apoptosis and translational repression of HIF-1[Formula: see text]. Taken together, osthole may be a potential agent in the treatment of colon cancer.
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Ali, Zainab M., Haitham Mahmood Kadhim, Omeed M. Hassan, Ammar Kubba, Zeena A. Hussein, and Hayder B. Sahib. "Antiangiogenic activity of 5-bromoindole carbothioamide derivative in ex vivo, in vivo, and in vitro experimental study." Pharmacia 71 (August 28, 2024): 1–9. http://dx.doi.org/10.3897/pharmacia.71.e128589.
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The study aimed to investigate the antiangiogenic, antioxidant, and cytotoxicity activity of a carbothioamide indole derivative. The 2-NPHC activity was evaluated using the ex vivo rat aorta ring assay, the in vivo chick chorioallantois membrane assay, the DPPH assay for scavenging activity, and the expression of the VEGF gene in colon cancer cell line (HCT116). The 2-NPHC had significant antiangiogenic activity in a dose-dependent manner in the rat aorta assay. 2-NPHC managed to reduce the DPPH free radical in a concentration-dependent, 2-NPHC had low to non-toxic effects on the HUVEC cell line, with an IC50 value of 711.7 μg/ml. The VEGF gene expression in the HCT116 cell line reduced the target gene expression compared to control cells. In conclusion, 2-NPHC exhibited significant inhibition of the angiogenesis process, either directly by inhibiting the release or activity of VEGF or indirectly through its antioxidant properties.
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Mun, Jeong-Geon, Hee Dong Jeon, Dae Hwan Yoon, et al. "Supercritical Extract of Cannabis sativa Inhibits Lung Metastasis in Colorectal Cancer Cells by Increasing AMPK and MAPKs-Mediated Apoptosis and Cell Cycle Arrest." Nutrients 14, no. 21 (2022): 4548. http://dx.doi.org/10.3390/nu14214548.
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Colorectal cancer (CRC) is one of the diseases with the highest rates of prevalence and mortality despite therapeutic methods in the world. In particular, there are not enough methods to treat metastasis of CRC cells to distant organs. Cannabis sativa Linne (C. sativa) is a popular medicinal plant used by humans to treat many diseases. Recently, extracts of C. sativa have shown diverse pharmacological effects as a result of choosing different extraction methods. In this study, we performed experiments to confirm the inhibitory effect and related mechanisms of supercritical extract of C. sativa on metastatic CRC cells. The effect of SEC on the viability of CRC cell lines, CT26 and HCT116, was determined using CCK reagent. Flow cytometry was performed to confirm whether SEC can promote cell cycle arrest and apoptosis. Additionally, SEC reduced proliferation of CT26 and HCT116 cells without causing toxicity to normal colon cell line CCD-18Co cells. SEC treatment reduced colony formation in both CRC cell lines, promoted G0/G1 phase arrest and apoptosis in CT26 and HCT116 cells through AMPK activation and MAPKs such as ERK, JNK, and p38 inactivation. Moreover, oral administration of SEC decreased pulmonary metastasis of CT26 cells. Our research demonstrates the inhibitory effect of SEC on CRC cell proliferation and metastasis. Thus, SEC might have therapeutic potential for CRC treatment.
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Alobaid, Hussah M., Maha H. Daghestani, Nawal M. AL-Malahi, Sabah A. Alzahrani, Lina M. Hassen, and Dina M. Metwally. "Exploring the effect of silver nanoparticles on gene expression in colon cancer cell line HCT116." Green Processing and Synthesis 11, no. 1 (2022): 1108–17. http://dx.doi.org/10.1515/gps-2022-0094.
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Abstract This study describes a new green method for silver nanoparticles (AgNPs) using Cymbopogon proximus (CP) extract and evaluates their potential anticancer properties in HCT116 cells. Ultraviolet-visible spectroscopy, transmission electron microscopy, dynamic light scattering, and Fourier transform infrared (FTIR) spectroscopy were used to successfully analyze the AgNPs. FTIR spectral analysis revealed the presence of phytochemicals that could be responsible for silver (Ag) ion reduction and AgNP capping. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay demonstrated that treating HCT116 cells with PC-AgNPs for 48 h caused cytotoxic effects, as evidenced by the existence of 20% cell viability. The RT-qPCR study revealed that the expression of two oncogenes (cathepsin B [CTSB] and epithelial cell adhesion molecule [EpCAM]) was significantly reduced in treated cells. The levels of various tumor suppressor genes, including adenomatous polyposis coli (APC), Beclin1 (BECN1), nuclear translocation of β-catenin (CTNNB1), low-density lipoprotein receptor-related protein 6, LRP5, TP53, and TNF, were dramatically reduced in cells treated with CP extract, but this was not the case in cells treated with CP extract. To conclude, CP-AgNPs have demonstrated their ability to induce cytotoxic action and exert antitumorigenic modulatory effects, particularly on the expression of CTSB and EpCAM in colon cancer cells, utilizing AgNPs as an antitumor therapeutic agent for 48 h is not recommended, and reducing the treatment time could be more effective.
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Srinivasalu, Vijay Kumar, Nazia Chaudhary, Bhagyashree ., et al. "LCN2 and colon cancer — Have we hit the jackpot." Journal of Clinical Oncology 38, no. 15_suppl (2020): e15608-e15608. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e15608.
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e15608 Background: Lipocalin2 (LCN2, also known as neutrophil gelatinase-associated lipocalin) is a protein that in humans is encoded by the LCN2 gene. Its abnormal expression serves critical roles in EMT transition, angiogenesis, cell migration and invasion in many cancers. We aim to assess the in vitro and in vivo effects of LCN2 as a potential chemo and radiosensitizer. Methods: Normalized RNAseq RSEM values of LCN2 were compared between normal and tumour samples from TCGA. Differences between median expression levels were assessed using Wilcoxon rank sum test. Kaplan-Meier model was used for survival analysis. Immune cell population in publicly available Colon Adenocarcinoma dataset was estimated using MCP Counter tool. Cell systems used to experimentally study the role of LCN2 in therapy resistance and tumor progression were HCT116, HT29 and DLD1. PKP3 and/or LCN2 were knocked down by shRNA. Tumor regression and therapy (5FU and radiation) sensitivity upon Anti-LCN2 treatment were demonstrated in Xenograft mouse models. Results: Analysis of 23 TCGA datasets containing gene expression data for both tumour and adjacent normal samples indicated that LCN2 levels are elevated in colon tumors. Colon cancer cell line HCT116 derived PKP3 knock-down or LCN2 over-expressing cells showed therapy resistance. A comparison of the tumor cell lines HCT116, HT29 and DLD1 show that increased LCN2 expression correlates with therapy resistance. LCN2 levels correlated with resistance to 5FU (p = 0.006) and its ability to clear ROS (p < 0.05) in vitro. Inhibiting LCN2 led to a decrease in invasion in vitro (p = 0.0005), increased sensitivity to 5FU in vitro (p = 0.001) and inhibition in tumor growth and increased sensitivity to 5FU and radiation (p = 0.005) in xenograft mouse models. On MCP counter analysis of TCGA, in Colon adenoca the normal samples show a correlation between LCN2 expression and T-cells (Pearson r = 0.45, p = 0.0028) and with the T-cell chemoattractant CXCL10 (Pearson r = 0.5, p < 0.0001). Such correlations are broken in tumour samples. Conclusions: LCN2 expression leads to chemo and radio resistance in colon cancer cell lines and xenograft mouse models. Inhibiting LCN2 function can inhibit tumor progression and sensitizes tumors to radiation and 5FU. These results suggest that LCN2 expression could be a marker that can be used to determine the choice of therapy offered to patients and that LCN2 could serve as a therapeutic target that sensitizes cells to radio and chemotherapy. LCN2 affects tumor progression and therapy sensitivity probably through T cell mediated immune pathway.