Bibliographies thématiques / Colon cancer cell line (HCT116)

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Littérature scientifique sur le sujet « Colon cancer cell line (HCT116) »

Auteur : Grafiati

Publié le 6 juin 2025

Mis à jour le 8 juin 2025

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Articles de revues sur le sujet "Colon cancer cell line (HCT116)"

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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