Gotowe bibliografie tematyczne / MCF-7 cells

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Gotowa bibliografia na temat „MCF-7 cells”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 5 lutego 2022

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Artykuły w czasopismach na temat "MCF-7 cells"

Men, Xin, Mengyang Su, Jun Ma, Yueyang Mou, Penggao Dai, Chao Chen i Xi An Cheng. "Overexpression of TMEM47 Induces Tamoxifen Resistance in Human Breast Cancer Cells". Technology in Cancer Research & Treatment 20 (1.01.2021): 153303382110049. http://dx.doi.org/10.1177/15330338211004916.

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Background: Tamoxifen (TAM) is the eminent first-line drug for endocrine therapy of hormone receptor positive premenopausal breast cancer and reduces the risk of recurrence by ∼50%. However, many patients developed TAM resistance and their diseases recurred. Our previous study on transcriptome profile of TAM resistant breast cancer cells revealed that the TMEM47 is one of the most significantly differentially expressed genes. The mechanism of how TMEM47 is involved in TAM resistance was not known. Methods: We constructed a mammal breast cancer cell line, in which TMEM47 was stably overexpressed (TMEM47-OE/MCF-7), to further verify the role of TMEM47 in TAM resistance. siRNA targeting TMEM47 was transfected into TAMR / MCF-7 cells by Liposome. TMEM47 expression was validated on mRNA and protein level by qRT-PCR and western blotting. We tested the cytotoxicity of TAM in the cells. Apoptosis was detected by flow cytometry. Results: Compared to the MCF7 cells, TMEM47 mRNA was significantly up regulated more than 6 folds in the TAMR/MCF7 cells and so its protein. TMEM47 expression level in TMEM47-OE/MCF-7 was similar as in the TAMR/MCF-7 cells. The 50% inhibitory concentration (IC50) value (mean ± SD) of TAM in MCF-7, TAMR/MCF-7 and TMEM47-OE/MCF-7 cells was 1.58 ± 0.19, 2.74 ± 0.24 and 3.12 ± 0.32 µγ/mL, respectively. The apoptosis rates of TAMR/MCF-7 and TMEM47-OE/MCF-7 cell lines were significantly lower than that of MCF-7 cells. After 24 and 48 hours TAM treatments, cell viability was significantly inhibitied in TMEM47 knockdown TAMR/MCF7 cells (P < 0.01). Consistant with the decreased cell viability, the apoptosis rate in TMEM47 knockdown TAMR/MCF-7 cells was significantly increased. Conclusions: Our results suggest that overexpression of TMEM47 in MCF-7 cells acquired TAM resistance to those cells, and knockdown of TMEM47 in TAMR/MCF-7 cells reversed their resistance to TAM. TMEM47 might confer TAM resistance on MCF-7 cells through the inhibition of apoptosis.

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Yang, Seungwon, i Hyun-Man Kim. "ROCK Inhibition Activates MCF-7 Cells". PLoS ONE 9, nr 2 (11.02.2014): e88489. http://dx.doi.org/10.1371/journal.pone.0088489.

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Chehkun, V. F., T. Borikun i N. Yu Lukianova. "EFFECT OF 5-AZACYTIDINE ON miRNA EXPRESSION IN HUMAN BREAST CANCER CELLS WITH DIFFERENT SENSITIVITY TO CYTOSTATICS". Experimental Oncology 38, nr 1 (22.03.2016): 26–30. http://dx.doi.org/10.31768/2312-8852.2016.38(1):26-30.

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Aim: To analyze expression of miRNA in human breast cancer cells, sensitive and resistant to cisplatin and doxorubicin, and to explore possible modification of drug sensitivity via treatment of cells with 5-azacytidine (5-aza), a demethylating agent. Materials and Methods: The study was performed on wild-type MCF-7 cell line (MCF-7/S) and its two sublines MCF-7/Dox and MCF-7/DDP resistant to doxorubicin and cisplatin, respectively. Cells were treated with 5-aza, cisplatin, doxorubicin and their combinations. Relative expression levels of miRNA-221, -200b, -320a, -10b, -34a, -122 and -29b were examined, using qRT-PCR. The MTT assay was used to monitor cell viability. Results: We compared miRNA expression profiles in MCF-7/S and drug resistant MCF-7/Dox and MCF-7/DDP cells. Changes of miRNA-221, -200b, -320a, -10b, -34a, -122 and -29b were observed in both resistant cell lines. The most significant differences were found for miRNA-200b (decreased in 50.0 ± 2.6 and 63.0 ± 3.1 times for MCF-7/Dox and MCF7/DDP cells, respectively) and for oncogenic miRNA-221 levels (increase in 62.0 ± 5.7 times for MCF-7/Dox and 83.8 ± 7.2 times for MCF-7/DDP cells). 5-aza treatment caused an increase of miRNA-10b, -122, -200b levels in MCF-7/S cells, miRNA-34a, -10b, -122, -200b and -320a levels in MCF-7/Dox cells and miRNA-34a, -10b, -200b and -320a levels in MCF-7/DDP cells. Pretreatment of all studied lines with 5-aza resulted in the increase of their sensitivity to studied cytostatics. In particular, the IC50 of doxorubicin decreased by 2-, 4- and 3-fold for cell lines MCF-7/S, MCF-7/Dox and MCF-7/DDP cells, respectively, and IC50 of cisplatin in studied cultures decreased by 3-, 2- and 1.5-fold, respectively. Conclusions: It was shown that use of 5-aza can modify sensitivity of breast cancer cells to cytotoxic drugs not only by it’s demetylation effect, but also by changes in expression of miRNAs, involved in cell proliferation, migration and drug resistance development.

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Huang, M., F. Zhang, Y. Xu, H. Wang, S. Lin i Y. Zhang. "The comparison of epirubicin-treated MCF-7 mammosphere cells to the treated monolayer cells". Journal of Clinical Oncology 27, nr 15_suppl (20.05.2009): e13542-e13542. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e13542.

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e13542 Objective: To explore the different effects of epirubicin on the MCF-7 mammosphere cells and the monolayer cells. Methods: MCF-7 cells were cultured in suspension to generate primary mammospheres. The inhibitory effects of epirubicin on MCF-7 mammosphere cells and the monolayer cells by were measured by MTT assay. The change of CD44+CD24- expression and cell cycle distribution in MCF-7 mammosphere cells and the monolayer cells under epirubicin condition was analyzed by flow cytometry. Results: The cell inhibition was lower in MCF-7 mammosphere cells than that in the monolayer cells when induced by the same concentration of epirubicin (>100 ng/ml),(P<0.01). The CD44+CD24- expression was significantly higher in MCF-7 mammosphere cells than that in the monolayer cells under 400 ng/μl epirubicin for 72 h, (22.8% ± 4.8% Vs 3.3% ± 0.8%),(P<0.01). The cell cycle indicated that MCF-7 mammosphere cells had higher proportion of G0/G1 phase than the monolayer cells, (74.33% ± 3.20% Vs 53.40% ± 3.45%) (P<0.01). Epirubicin had little effect on the G0/G1 phase of MCF-7 mammosphere cells and the monolayer cells, but the S phase and G2 phase was not the case. Conclusion: Epirubicin had lower inhibitory effects on MCF-7 mammosphere cells and it can be used to enrich breast cancer stem cell. Epirubicin had lower effect on the G0/G1 phase of MCF-7 mammosphere cells as compared with control. No significant financial relationships to disclose.

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Alkreathy, Huda Mohammed, Noura Farraj AlShehri, Fatemah Omer Kamel, Ahmed Khalaf Alghamdi, Ahmed Esmat i Shahid Karim. "Aged garlic extract potentiates doxorubicin cytotoxicity in human breast cancer cells". Tropical Journal of Pharmaceutical Research 19, nr 8 (19.11.2020): 1669–76. http://dx.doi.org/10.4314/tjpr.v19i8.15.

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Purpose: To investigate the potential chemo-sensitizing effect of aged garlic extract (AGE) on doxorubicin (DOX) in breast cancer cells (MCF-7), and the possible underlying mechanisms.Methods: Human breast cancer cell line (MCF-7) was treated with AGE and DOX. The cytotoxic effects of AGE and DOX were investigated via cell cycle analysis and apoptosis induction, using flow cytometry. Mechanistic studies involved the determination of cellular uptake of DOX and p-glycoprotein (P-gp) activity.Results: Combined treatment of MCF7 cells with AGE and DOX produced no significant effect at AGE dose of 10 mg/mL. However, co-treatment with AGE at doses of 50 and 93 mg/mL enhanced the cytotoxicity of DOX on MCF-7 cells, with IC50 values of 0.962 and 0.999 μM, respectively, whencompared with 1.85 μM DOX alone. Moreover, Annexin V-FITC and PI techniques showed that AGE significantly increased percentage of cells in late apoptosis. Besides, AGE-DOX treatment significantly increased cellular uptake of DOX and inhibited P-gp activity, when compared with DOX alone (p < 0.05).Conclusion: AGE enhances the cytotoxic effect of DOX on MCF-7 cells, most likely due to cell cycle distribution, stimulation of apoptosis, increased uptake of DOX by MCF7, and inhibition of P-gp activity. Keywords: Aged garlic extract, Doxorubicin, Breast cancer, MCF-7 cell line, P-glycoprotein, Apoptosis, Cell cycle

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Gelmann, Edward P., Erik W. Thompson i Connie L. Sommers. "Invasive and metastatic properties of MCF-7 cells andrasH-transfected MCF-7 cell lines". International Journal of Cancer 50, nr 4 (20.02.1992): 665–69. http://dx.doi.org/10.1002/ijc.2910500431.

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Kars, Meltem Demirel, Özlem Darcansoy Iseri, Ali Ugur Ural, Ferit Avcu, Murat Beyzadeoglu, Bahar Dirican i Ufuk Gündüz. "Development of radioresistance in drug resistant human MCF-7 breast cancer cells". Journal of Radiotherapy in Practice 8, nr 4 (grudzień 2009): 207–13. http://dx.doi.org/10.1017/s1460396909990070.

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AbstractBackground and purpose: Radiotherapy is used for the treatment of malignant tumours, and may be used as the primary therapy. It is also common to combine radiotherapy with surgery, chemotherapy, hormone therapy or some combination of them. Even if the tumour is treated intensively, women diagnosed with breast cancer may develop a recurrence. Most recurrences may be in the form of distant metastases, development of multi-drug resistance phenotype or both together. This study demonstrated that some of the multi-drug resistant cancer cells may also become radioresistant.Materials and Methods: Chemoresistance in paclitaxel (MCF-7/Pac), docetaxel (MCF-7/Doc), vincristine (MCF-7/Vinc), doxorubicin (MCF-7/Dox) and zoledronic acid (MCF-7/Zol) resistant MCF-7 cells were demonstrated by XTT assay. MDR1 gene expression was detected by real-time PCR in human MCF-7 breast cancer cells. Drug resistant and sensitive cells were exposed to γ-radiation and development of radioresistance was investigated.Results: Results have indicated that paclitaxel, docetaxel, vincristine, doxorubicin and zoledronic acid–selected cells gained varying degrees of resistance to their selective drugs when compared with original MCF-7/S. MCF-7/Pac, MCF-7/Doc, MCF-7/Vinc and MCF-7/Dox cells have all acquired MDR1 expression. Among the resistant sub-lines, MCF-7/Pac and MCF-7/Doc cells were significantly cross-resistant to irradiation compared to the sensitive cells.Conclusion: MCF-7/Pac and MCF-7/Doc cell lines were found radioresistant to γ-radiation. On the contrary, doxorubicin, vincristine and zoledronic acid resistant cancer cells were still sensitive to radiation.

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Song, Ting, Furong Liang, Zhichao Zhang, Yubo Liu, Hongkun Sheng i Mingzhou Xie. "S1 kills MCF-7/ADR cells more than MCF-7 cells: A protective mechanism of endoplasmic reticulum stress". Biomedicine & Pharmacotherapy 67, nr 8 (październik 2013): 731–36. http://dx.doi.org/10.1016/j.biopha.2013.03.015.

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Putri, Dyaningtyas Dewi Pamungkas, Sarmoko Sarmoko, Rifki Febriansah, Endah Puspitasari, Nur Ismiyati i Aditya Fitriasari. "MCF-7 Resistant Doxorubicin are Characterized by Lamelapodia, Strong Adhesion on Substrate and P-gp Overexpression". Indonesian Journal of Cancer Chemoprevention 2, nr 3 (31.10.2011): 304. http://dx.doi.org/10.14499/indonesianjcanchemoprev2iss3pp304-309.

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The prognosis of breast cancer patients is closely associated with the response of tumor cells to chemotherapy agent. Doxorubicin is one of the primary chemotherapeutic agents used for the treatment of breast cancer. Resistance to chemotherapy is believed to cause treatment failure in cancer patients. Furthermore, long time exposure to chemotherapeutic agent induces cancer cells resistance. MCF-7 sensitive cells used as chemoresistance model have overexpression P-gp (P-glycoprotein). Chemoresistance was established by treating MCF-7 cells with 0.5 µg/ml doxorubicin-contained medium for a week. 50% inhibiting concentration (IC50) doxorubicin on MCF-7 cells/DOX were determined using MTT assay. Western blot assay and immunocytochemistry assay was performed to determine the expression of P-gp. Morphological of MCF-7 cell/DOX was changing to become larger and have lamellapodia. IC50 value of doxorubicin was 700 nM on MCF-7/DOX and 400 nM on sensitive MCF-7 cells. The MCF-7/DOX sensitivity to doxorubicin was decreased, shown by 1.5 fold higher IC50 of doxorubicin on MCF-7/DOX compared to MCF-7 sensitive cells. Treatment doxorubicin to sensitive MCF-7 cells leads to the increasing P-gp expression. The P-gp level expression has strong correlation with the low sensitivity of MCF-7/DOX to doxorubicin.Keywords: doxorubicin, resistance cells, sensitive MCF-7 cell

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Guo, Qingming, Danni Zhu, Xiaocui Bu, Xiaofang Wei, Changyou Li, Daiqing Gao, Xiaoqiang Wei, Xuezhen Ma i Peng Zhao. "Efficient killing of radioresistant breast cancer cells by cytokine-induced killer cells". Tumor Biology 39, nr 3 (marzec 2017): 101042831769596. http://dx.doi.org/10.1177/1010428317695961.

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Recurrence of breast cancer after radiotherapy may be partly explained by the presence of radioresistant cells. Thus, it would be desirable to develop an effective therapy against radioresistant cells. In this study, we demonstrated the intense antitumor activity of cytokine-induced killer cells against MCF-7 and radioresistant MCF-7 cells, as revealed by cytokine-induced killer–mediated cytotoxicity, tumor cell proliferation, and tumor invasion. Radioresistant MCF-7 cells were more susceptible to cytokine-induced killer cell killing. The stronger cytotoxicity of cytokine-induced killer cells against radioresistant MCF-7 cells was dependent on the expression of major histocompatibility complex class I polypeptide–related sequence A/B on radioresistant MCF-7 cells after exposure of cytokine-induced killer cells to sensitized targets. In addition, we demonstrated that cytokine-induced killer cell treatment sensitized breast cancer cells to chemotherapy via the downregulation of TK1, TYMS, and MDR1. These results indicate that cytokine-induced killer cell treatment in combination with radiotherapy and/or chemotherapy may induce synergistic antitumor activities and represent a novel strategy for breast cancer.

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Rozprawy doktorskie na temat "MCF-7 cells"

Khurshid, Asma. "The effect of the polyadenylation inhibitor Cordycepin on MCF-7 cells". Thesis, University of Nottingham, 2015. http://eprints.nottingham.ac.uk/28835/.

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Cordycepin (3′-deoxyadenosine) is a medicinal bioactive component of the caterpillar fungi (Cordyceps and Ophicordyceps). It is reported to have nephroprotective, antiapoptotic, anti-metastatic, hepatoprotective (Yue et al. 2013), inflammatory effects, antioxidant, anti-tumor, immunomodulatory and vasorelaxation activities. Cordycepin is well known to terminate and inhibit polyadenylation, both in vitro and in vivo. Other proposed mechanisms of action of cordycepin include activation of adenosine receptors, activation of AMP dependent kinase (AMPK) and inhibition of PARP1. The purpose of this study is to elucidate the biological and pharmacological effects of cordycepin on cancer cell lines such as MCF-7 cells. In this study I found that cordycepin reduces the cell proliferation in all examined cell lines without always exerting an effect on 4EBP phosphorylation and protein synthesis rates. Therefore, the effects on protein synthesis via inhibition of mTOR, which were previously reported, are not only the sole reason for the effect of cordycepin on cell proliferation. Knockdown of poly (A) polymerases reduces cell proliferation and survival, indicating that poly (A) polymerases are potential targets of cordycepin. I studied different adenosine analogues and found that 8 aminoadenosine, the only one that also consistently inhibits polyadenylation, also reduces levels of P-4EBP. It also inhibits the expression of specific genes indicating that the effects on polyadenylation, mTOR signalling and gene expression are linked. Also consistent with polyadenylation inhibition as the major mode of action is the fact that the effects of cordycepin on gene expression are predominantly post-transcriptional. However, knockdown of poly (A) polymerases did not have the same effects on gene expression or on polyadenylation, indicating that cordycepin may act as a dominant negative rather than as a null mutant. This is consistent with the fact that cordycepin is known to arrest a normally transient polyadenylation complex. We performed microarray analysis of cordycepin treated MCF-7 cells and found that the downregulated mRNAs were predominantly involved in transcriptional regulation, cell proliferation, cell cycle and cell migration. These data show that cordycepin is a promising new drug for cancer and indicates that the mode of action it is likely to be through the inhibition of polyadenylation.

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Eng, Jamei Raena. "Localization of anthracyclines in drug resistant human MCF-7 breast cancer cells". Thesis, University of Ottawa (Canada), 2007. http://hdl.handle.net/10393/27841.

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Multidrug resistance (MDR) commonly occurs during the treatment of cancer. Current research has focused mostly on the role of drug transporters, as the main mechanism of MDR; however, few have demonstrated a definite link between the expression or function of drug transporters and MDR in cancer patients. Anthracyclines such as doxorubicin and epirubicin, autofluoresce and can be monitored by confocal microscopy. Two of the four resistant cell fines generated in our lab: the MCF-7EPI cells and to some extent MCF-7 DOX cells, exhibit a localization defect, whereby epirubicin is localized primarily in the cytoplasm rather than the nucleus. This drug localization defect temporally correlated with the onset of drug-resistance during selection for drug resistance in these cell lines. Consistent with the possible sequestration of drugs into acidic vesicles, acridine orange staining has revealed the presence of aggregates of acidified vesicles in the perinuclear region of MCF-7EPI cells. However, co-localization experiments using a number of intracellular organelle markers determined that epirubicin was localized to lysosomes and not consistently to acidic vesicles. An inhibitor of vacuolar H+ ATPase, was unable to restore the localization of epirubicin to the nucleus. Immunofluorescence using an ABCB1 antibody revealed the localization of ABCB1 predominantly in the plasma membrane and to some extent in the perinuclear region of MCF-7EPI cells. Nevertheless, inhibitors of this transporter failed to restore localization of epirubicin to the nucleus. Taken together, these findings strongly suggest that the acquisition of epirubicin resistance in breast tumour cells may involve the P-glycoprotein independent sequestration of drug into lysosomes. These lysosomes need not be acidic, nor does the removal of acid vesicles by inhibition of vacuolar H+ ATPases block the sequestration of drug into lysosomes.

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Pfeiffer, Thomas J. "Phytoestrogens may inhibit proliferation of MCF-7 cells, an estrogen-responsive breast adenocarcinoma cell line". Link to electronic thesis, 2004. http://www.wpi.edu/Pubs/ETD/Available/etd-0430104-132238.

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Tezcan, Okan. "Metastatic Behaviour Of Doxorubicin Resistant Mcf-7 Breast Cancer Cells After Vimentin Silencing". Master's thesis, METU, 2013. http://etd.lib.metu.edu.tr/upload/12615553/index.pdf.

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Chemotherapy is one of the common treatments in cancer therapy. The effectiveness of chemotherapy is limited by several factors one of which is the emergence of multidrug resistance (MDR). MDR is caused by the activity of diverse ATP binding cassette (ABC) transporters that pump drugs out of the cells. There are several drugs which have been used in treatment of cancer. One of them is doxorubicin that intercalates and inhibits DNA replication. However, doxorubicin has been found to cause development of MDR in tumors. It has been reported that there is a correlation between multidrug resistance and invasiveness of cancer cells. Vimentin is a type III intermediate filament protein that is expressed frequently in epithelial carcinomas correlating with invasiveness and also poor prognosis of cancer. There are several studies that have shown the connection between expression level of vimentin and invasiveness. In this study, MCF-7 cell line (MCF-7/S), which is a model cell line for human mammary carcinoma, and doxorubicin resistant MCF-7 cell line (MCF-7/Dox) were used. The resistant cell line was previously obtained by stepwise selection in our laboratory. The main purpose of this study was to investigate changes of metastatic behaviour in MCF-7/Dox cell line, after transient silencing of vimentin gene by siRNA. In conclusion, down-regulation of vimentin gene expression in MCF-7/Dox cell lines was expected to change the characteristics in migration and invasiveness shown by migration and invasion assays.

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Miazga, Natalie. "The effects of exogenous E-cadherin inhibition in MCF-7 mammary epithelial cells". Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/the-effects-of-exogenous-ecadherin-inhibition-in-mcf7-mammary-epithelial-cells(e17fb558-8dcf-48ed-b095-5e28ea45c3b9).html.

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Understanding mechanisms that contribute to tumorigenesis and metastasis is important for developing more effective cancer therapies. Epithelial-mesenchymal transition (EMT) is associated with loss of the cell surface protein E-cadherin, increased tumour cell metastasis and acquisition of a cancer stem cell (CSC) phenotype. Whilst the process of EMT and aberrant E-cadherin expression during metastasis have been studied in detail, the role of exogenous inhibition of E-cadherin protein alone in epithelial cells remains to be elucidated. In this study the E-cadherin neutralising antibody SHE78.7 (nAb) and a peptide inhibitor of E-cadherin (nPep) have been used to assess how alterations in cell surface E-cadherin affect adenocarcinoma cell line MCF-7. MCF-7 cells exhibit an epithelial phenotype characterised by cell surface E-cadherin expression and lack of EMT marker expression, such as N-cadherin and Vimentin. Exogenous inhibition of cell surface E-cadherin using nAb in MCF-7 cells is a reversible process which induces increased cell numbers due to decreased apoptosis and cell proliferation. However, nAb treatment was insufficient to induce EMT or a CSC phenotype. Treatment of MCF-7 cells with nPep also induced increased cell numbers, but this was due to increased proliferation of the cells, with no changes in apoptosis observed. Microarray analysis of nAb-treated MCF-7 cells revealed >1000 gene transcript alterations compared to control Ab-treated cells, with changes associated with a wide range of cellular functions. Using an in silico network analysis approach, E-cadherin was identified as a positive regulator of the histone acetyltransferase p300. Exposure of MCF-7 cells to the p300 inhibitor garcinol resulted in increased CD44 and Slug, and decreased CD24 CSC associated transcripts. nPep treatment of MCF-7 cells and subsequent high content screening (HSC) analysis following exposure to a panel of cancer therapeutics demonstrated increased drug efficacy in combination with nPep for most of the therapeutics. Furthermore, nPep-treated MCF-7 cells exhibited a significantly altered plasma membrane-associated protein profile compared to control cells. Together, these results show that exogenous inhibition of E-cadherin in MCF-7 cells is a reversible event associated with increased proliferation, reduced apoptosis and significantly altered protein and transcript expression that may contribute to neoplasm formation in vivo. Furthermore, I show for the first time that inhibition of p300-dependent gene transactivation induces a CSC gene transcript expression profile in MCF-7 cells in vitro.

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Kanwal, Shahzina. "Effect of O-GlcNAcylation on tamoxifen sensitivity in breast cancer derived MCF-7 cells". Phd thesis, Université René Descartes - Paris V, 2013. http://tel.archives-ouvertes.fr/tel-00912341.

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One of the hallmarks of cancer cells is to exhibit increased uptake and consumption of glucose.3-5% of the glucose entering into the cell leads to a minor pathway of the glucose metabolismknown as the hexosamine biosynthetic pathway (HBP). UDP-N-acetylglucosamine is the endproduct of HBP and is used as substrate by OGT (O-GlcNAc transferase) to modify diverserange of nuclear and cytoplasmic proteins with a recently characterized post-translationalmodification called O-GlcNAcylation. It corresponds to the addition of sugar moiety O-linked β-N-acetylglucosamine (O-GlcNAc) on serine or threonine residue of proteins. This process isantagonized by another enzyme called O-GlcNAcase (OGA). Recent studies indicated thepresence of increased O-GlcNAcylation level in several cancer cells. Moreover, inhibition ofOGT has been shown to reduce in vivo and in vitro tumor growth of breast cancer cells.However, the relationship between O-GlcNAcylation and the response to anti-cancer therapy hasnot been studied. Tamoxifen is the oldest and most prescribed selective-estrogen receptormodulator (SERM) for patients with estrogen receptor (ER)-positive breast cancer. Tamoxifen isknown to reduce tumor growth and invasion. Despite its beneficial effects de novo and acquiredresistance are great obstacles in its clinical effectiveness. We found that O-GlcNAc elevation inMCF-7 cells protected them from tamoxifen-induced cell death. Increased O-GlcNAc alsoincreased PI3-K/Akt signaling. However, the protective effect of PUGNAc+glucosamine fromtamoxifen-induced cell death is independent of PI3K/Akt pathway. Increased O-GlcNAcylationalso led to reduced ESR1 promoter activity and decreased expression of ERα at mRNA andprotein levels. The decrease in ERα expression is correlated with a reduced expression of twotamoxifen regulated genes i.e. early growth response 1 and p21 Waf1/Cip1. In conclusion, thisstudy showed for the first time the involvement of O-GlcNAcylation in reducing tamoxifen142sensitivity in MCF-7 cells. Thus, OGT can act as a novel therapeutic target for treatment oftamoxifen resistant cells.

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Qattan, A. T. M. "Large scale quantitative organelle proteomics of protein distribution in breast cancer MCF-7 cells". Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1415963/.

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This thesis analyzes the dynamic complexity involved in the subcellular distribution of the proteins for the malignant breast epithelial MCF-7 cell line, using mass spectrometry based quantitative proteomics for the indirect measurement of the subcellular dispersion of the constituent proteins of core cellular functions. The thesis demonstrates that there are many proteins which can be present in more than one subcellular organelle. Quantitative proteomics using LFQP (Label-Free Quantitative Proteomics) methodology based on mass spectrometry was shown to be suitable for the indirect measurement of the distribution of the proteins in the malignant breast epithelial cell line. The study used partial purification by means of dynamic sucrose gradient centrifugation to avoid the need of multiple purification procedures for different organelles and loss of proteins during purification. This was followed by proteomics identification and analysis of the protein content from the sucrose gradient fractions corresponding to the major organellar compartment. These included the nucleus, cytosol, mitochondria, plasma membrane and endoplasmi c reti cul um. The first part of the thesis indicates that 50.00% - 75.00% of the proteins detected showed multiple-locations. Out of the total quantified proteome using LFQP methodology, 2184 proteins were securely identified. 481 proteins (22.00%) were found in unique sucrose gradient fractions which suggest that they may have unique locations, while 454 proteins (20.80%) were found to be ubiquitously distributed and the remaining 1249 proteins (57.20%) were consistent with intermediate distribution over multiple locations. 94 proteins implicated in breast cancer and 478 other proteins which share the same major cellular biological processes with most of the breast cancer proteins were observed in 334 and 1223 subcellular locations respectively. The second part of the thesis concentrates on the spatial distribution of proteins between two organelles of particular interest for cancer: the nucleus and mitochondria. Two important characteristics of cancer cellular function include high degrees of genetic instability and major changes in cellular energy metabolism. The genetic instability, which is associated with the cell nucleus, allows cells to escape from a variety of normal restrictions on proliferation, whereas the changes in energy metabolism are associated with mitochondria and the need for new cellular components to be produced in the proliferating cells. The large scale proteomics analysis of the partitioning of proteins between mitochondria and the nucleus reveals that 40.00% of all the proteins were shared between the mitochondria and the nucleus. The observed partitioning of these proteins between these two organelles showed a functional distribution which is consistent with the first part of the thesis. The analysis of the distribution between the nucleus and mitochondria of specific subgroups of the proteins involved in oxidative phosphorylation, the tricarboxylic acid cycle, RNA processing/translation, glycolysis and Ras-related signalling suggests that the spatial distribution of numerous proteins over multiple sites is critical to cellular function and that there are unrecognized aspects of functional coordination between the mitochondria and the nuclei which need further investigation. In addition, the large number of proteins identified to be in multiple locations indicates that subcellular spatial integration of function may be a vital aspect of cancer. The findings in this study also reveal that most of the observed proteins with multiple subcellular locations had current annotations of location which are still sparse in public databases. In general terms, the extensive subcellular dispersion of the constitute proteins of core cellular functions may be a fundamental feature of the cell which may be constituent with the requirements for robustness in a complex system.

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Wood, Rachel. "The effects of JNK isoform knockdown on cell growth and death in HUVECs and MCF-7 cells". Thesis, University of Strathclyde, 2017. http://digitool.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=27904.

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Cardiovascular disease (CVD) and cancer are two of the leading causes of mortality worldwide. The JNK pathway has been shown to play key roles at various stages of both of these diseases and therefore is an important protein to try and understand. In animal models of atherosclerosis and breast cancer, inhibition of JNK has been demonstrated to reduce pathogenesis and therefore targeting this protein may be key for developing treatments. JNK exists as three individual proteins, JNK1, JNK2 and JNK3 and studies are now showing that not only can these proteins work independently but also opposingly in some instances and therefore understanding the function of the individual isoforms is becoming critical to fully understanding this pathway. Although more research is focusing on JNK isoform function, characterisation of each JNK protein has not yet been carried out in human primary vascular cells or a human breast cancer cell line, an investigation which must be carried out to understand the role of this pathway in the pathogenesis of these diseases. In the current study lentiviral shRNA was used to target and knockdown JNK1 and JNK2 in both human umbilical vein endothelial cells (HUVECs) and MCF-7 breast cancer cells and the effects of knockdown on cell growth and cell death processes were analysed. In HUVECs knockdown of JNK2 caused an increase in pc-Jun levels and an increase in the percentage of multinucleated cells was observed, suggesting JNK2 may play a role in HUVEC cell growth. Unfortunately, the lentiviral infection itself caused detrimental effects which made it difficult to continue experiments and explore these findings further. In MCF-7 cells JNK knockdown did not produce any changes in cell growth or induced cell death when compared to non-target controls, suggesting that JNK does not play a key role in this breast cancer cell line.

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Fix, Lindsey Zhang Baohong. "Effect of green tea Polyphenon 60 on microRNA expression in MCF-7 breast cancer cells". [Greenville, N.C.] : East Carolina University, 2010. http://hdl.handle.net/10342/2725.

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Husbeck, Bryan. "Changes in gene expression induced by thioredoxin-1 in MCF-7 human breast cancer cells". Diss., The University of Arizona, 2002. http://hdl.handle.net/10150/280113.

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Thioredoxin-1 (Trx-1) is a small redox protein that is overexpressed in a number of human cancers. Elevated levels of Trx-1 in tumors is associated with increased cell proliferation, decreased apoptosis, and decreased patient survival. However, the mechanism(s) for the growth stimulating and anti-apoptosis effects of Trx-1 are unknown. We used DNA microarray technology to identify genes whose expression was altered in MCF-7 breast cancer cells stably transfected with wild-type Trx-1 (MCF-7/Trx 9) or a redox inactive mutant Trx-1 (MCF-7/SerB 4) compared to empty-vector transfected cells (MCF-7/neo). The expression of cytochrome P450 1B1 (CYP1B1) mRNA and protein is increased by Trx-1 transfection of MCF-7 human breast cancer cells and decreased by a redox inactive mutant Trx-1. CYP1B1 is a tumor specific CYP which converts 17β-estradiol (E₂) to the carcinogenic 4-hydroxyestradiol (4-OHE₂). The expression of peroxiredoxin 1 (PRDX1) mRNA is increased as a result of Trx-1 overexpression in MCF-7 cells. The peroxiredoxins belong to a conserved family of antioxidant proteins that use thiol groups as reducing equivalents to scavenge oxidants. Transfection of mouse WEHI7.2 thymoma cells with human PRDX1 protects cells from apoptosis induced by H₂O₂. Spermine/spermidine N'-acetyltransferase (SSAT) mRNA expression and enzyme activity is decreased by Trx-1 transfection of MCF-7 human breast cancer cells. SSAT is an important enzyme in the polyamine catabolic pathway. The inhibition of SSAT enzyme activity is associated with decreased putrescine levels in the Trx-1 transfected cells. Therefore, it appears as if the modification of cellular redox signaling brought about by the overexpression of Trx-1 in breast cancer cells induces changes in gene expression that contribute to the transformed phenotype. Trx-1 redirects estrogen metabolism in a more toxic pathway due to the induction of CYP1B1, provides resistance to apoptosis induced by reactive oxygen species via the upregulation of PRDX1, and alters polyamine metabolism by inhibiting the expression of SSAT.

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Książki na temat "MCF-7 cells"

Mailloux, Jeremy. The Effects of DMSO (Dimethyl Sulfoxide) on MCF-7 breast carcinoma cells. Sudbury, Ont: Laurentian University, 1999.

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Bourgeault, Geoffrey A. Energy metabolism of wild type MCF-7 human breast cancer cells and its adriamyacin resistant derivative. Sudbury, Ont: Laurentian University, 1997.

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Hodgins, Tanya. The effects of dimethyl sulfoxide on the energy metabolism of MCF-7-ADR breast carcinoma cells. Sudbury, Ont: Laurentian University, 2000.

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Dickie, Sean. Initial study of the metabolism of glutamine in the isolated mitochondria of human MCF-7 breast cancer cells. Sudbury, Ont: Laurentian University, 1999.

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Gannon, Brian R. Dominant inhibition of cyclic AMP - dependent protein kinase in MCF-7 breast cancer cells: Effects on multidrug resistance. Sudbury, Ont: Laurentian University, 1997.

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Steinberg, Ken. Effects of structural domains of Raf-1 on the sensitivity of MCF-7 breast cancer cells to Taxol (Paclitaxel). Sudbury, Ont: Laurentian University, School of Graduate Studies, 2005.

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Huq, Rokaiya. Energy metabolism in human MCF-7 ADR and ADR-9 breast cancer cells treated with P-glycoprotein inhibitor PSC 833. Sudbury, Ont: Laurentian University, 2000.

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Olsten, Mary Ellen. The effect of PSC 833 on the energy metabolism of human MCF-7 ADR and ADR-B breast cancer cells. Sudbury, Ont: Laurentian University, 2000.

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Gannon, Brian Robert. The role of camp-dependent protein kinase in the expression and function of p-glycoprotein and other molecules implicated in drug resistance in adriamycin-resistant MCF-7 human breast cancer cells. Sudbury, Ont: Laurentian University, Chemistry and Biochemistry Department, 1999.

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Wijesuriya, Kanchana. Limiting glucose concentrations in human breast cancer cell lines, MCF-7/WT and MCF-7/ADR. Sudbury, Ont: Laurentian University, 1998.

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Części książek na temat "MCF-7 cells"

Ruh, T. S., M. F. Ruh i R. K. Singh. "Antiestrogen Action in MCF-7 Cells". W Receptor Mediated Antisteroid Action, redaktor M. K. Agarwal, 307–28. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110846935-013.

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Finlay, Thomas H., Susan S. Kadner i Snait Tamir. "Protease Inhibitor Synthesis by MCF-7 Breast Cancer Cells". W Protease Inhibitors as Cancer Chemopreventive Agents, 141–59. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2882-1_8.

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Han, Xiaobin, Andrea Budreau Patters i Russell W. Chesney. "Transactivation of TauT by p53 in MCF-7 Cells". W Advances in Experimental Medicine and Biology, 139–47. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0077-3_18.

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Silva, J. G., J. Maldonado, J. S. Tapia, N. E. Herrera, S. M. Polo, S. G. Martínez i C. A. González. "Selective Targeting of Breast Cancer Cells MCF-7 by Ferromagnetic Nanoparticles". W V Latin American Congress on Biomedical Engineering CLAIB 2011 May 16-21, 2011, Habana, Cuba, 983–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-21198-0_250.

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Zhang, Xue-Min, i De-Hui Chen. "Effect of Estradiol on MCF-7 Human Breast Cancer Cells: Ultrastructural Studies". W Hormonal Carcinogenesis II, 410–13. New York, NY: Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4612-2332-0_55.

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Wagner, Jörg, Ling Jiang i Leane Lehmann. "Phytoestrogens Modulate the Expression of 17α-Estradiol Metabolizing Enzymes in Cultured MCF-7 Cells". W Hormonal Carcinogenesis V, 625–32. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_65.

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Luo, Xuegang, Chunling Zhang, Wenwen Zhao, Lei Liu, Shu Guo, Zhipeng Liu, Jing Wang i Tong-Cun Zhang. "MRTF-A Promotes Migration of MCF-7 Breast Cancer Cells via Transactivation of CYR61". W Proceedings of the 2012 International Conference on Applied Biotechnology (ICAB 2012), 821–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-37922-2_86.

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Tachiiri, Seiji, Hiraku Takebe, Masahiro Hiraoka i Junji Miyakoshi. "Magnetic Fields (60Hz, 5mT) Do Not Influence MCF-7 Growth in Melatonin Insensitive Cells". W Electricity and Magnetism in Biology and Medicine, 841–43. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4867-6_201.

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Simboli-Campbell, M., i J. Welsh. "1,25 Dihydroxyvitamin D3: Coordinate Regulator of Active Cell Death and Proliferation in MCF-7 Breast Cancer Cells". W Apoptosis in Hormone-Dependent Cancers, 181–200. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-03122-3_10.

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Welsh, JoEllen, Maura Simboli-Campbell, Carmen J. Narvaez i Martin Tenniswood. "Role of Apoptosis in the Growth Inhibitory Effects of Vitamin D in MCF-7 Cells". W Advances in Experimental Medicine and Biology, 45–52. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-0949-7_4.

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Streszczenia konferencji na temat "MCF-7 cells"

Zhou, Fuyuan, Wenxue Wang i Lianqing Liu. "Discrimination of the state of MCF-7 cells by multiple cell mechanics". W 2016 IEEE International Conference on Cyber Technology in Automation, Control, and Intelligent Systems (CYBER). IEEE, 2016. http://dx.doi.org/10.1109/cyber.2016.7574871.

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Richardson, Adam D., Shuqian Liu i Jeffrey A. Moscow. "Abstract 35: Metabolomic analysis of MCF-7 and MCF-10 cells after thiaminase I exposure". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-35.

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Fadhel, Muhannad N., Elizabeth S. L. Berndl, Eric M. Strohm i Michael C. Kolios. "Ultra-high frequency acoustic impedance maps of MCF-7 cells". W 2014 IEEE International Ultrasonics Symposium (IUS). IEEE, 2014. http://dx.doi.org/10.1109/ultsym.2014.0475.

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Berg, Patricia E., Sanket Awate, Saurabh Kirolikar i Arnold Schwartz. "Abstract 1200: BP1 regulates ERα activity in MCF-7 cells". W Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1200.

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Pu, Hongping, Xiaodong Ma, Zhixiang Xu, Jun Liu, Bin Huang, Dong Ren, Huan He i Xuejun Pan. "Estrogenic Joint Effect of BPA and DES on MCF-7 Cells". W 2016 5th International Conference on Advanced Materials and Computer Science (ICAMCS 2016). Paris, France: Atlantis Press, 2016. http://dx.doi.org/10.2991/icamcs-16.2016.181.

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Yoshimoto, T., T. Ishikawa, N. Matsuki, H. Fujiwara, Y. Imai, H. Ueno, M. Takeda i T. Yamaguchi. "Rheology of Cancer Cells With Different Metastatic Properties". W ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206593.

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Cancer is the leading cause of death in Japan as well as many other countries. One of the most serious problem of cancer is that cancer cells often migrate to a distant part of the body, referred to as metastasis. The rheological properties of cancer cells have been investigated by some reserchers [1,2]. However, the correlations between the metastasis and the rheological properties are still unclear, because of limited number of experimental cases reported so far. In this study, we used two kinds of human breast cancer cell lines, MCF-7 and KPL-4. It is known that KPL-4 has much higher metastatic property than MCF-7. The rheological properties of these cells were measured by a micropipette aspiration method [3,4]. By comparing Young’s modulus between two kinds of cancer cells, we discuss the correlations between the metastasis and the cell deformability.

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Elfar, Mahmoud, Mariam Ayoub, Aya Sameh, Hazem Abass, Reham M. Abdel-Kader, Iman Gomaa i Islam S. M. Khalil. "Targeted penetration of MCF-7 cells using iron-oxide nanoparticles in vitro". W 2016 6th IEEE International Conference on Biomedical Robotics and Biomechatronics (BioRob). IEEE, 2016. http://dx.doi.org/10.1109/biorob.2016.7523635.

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Amin, Indah Mohd, Siti H. Sheikh Abdul Kadir, Nik Mohd Mazuan Nik Mohd Rosdy, Rosfaiizah Siran i Narimah A. H. Hasani. "Anti-cancer effect of aloe emodin on breast cancer cells, MCF-7". W 2013 7th International Conference on Systems Biology (ISB). IEEE, 2013. http://dx.doi.org/10.1109/isb.2013.6623802.

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Sil, Sukanya M., Huijun Yuan i Nanette H. Bishopric. "Abstract LB-135: The transcriptome of p300 loss in MCF-7 cells". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-135.

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"Calreticulin Overexpression Suppresses Cell Proliferation and Enhances Apoptosis on Human MCF-7 Breast Cancer Cells". W International Conference on Chemical, Agricultural and Medical Sciences. International Institute of Chemical, Biological & Environmental Engineering, 2013. http://dx.doi.org/10.15242/iicbe.c1213012.

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Raporty organizacyjne na temat "MCF-7 cells"

Sachdeva, Mandip S. Reversal of Doxorubicin Resistance in Human Breast Adenocarcinoma (MCF-7) Cells by Liposomal Monensin. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2005. http://dx.doi.org/10.21236/ada443420.

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Petz, Lawrence N. Expression of the Estrogen-Regulated pS2 Gene in MCF-7 Human Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2001. http://dx.doi.org/10.21236/ada398062.

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Sachdeva, Mandip S., i Krishna Agrawal. Reversal of Doxorubicin Resistance in Human Breast Adenocarcinoma (MCF-7) Cells by Liposomal Monensin. Fort Belvoir, VA: Defense Technical Information Center, maj 2002. http://dx.doi.org/10.21236/ada405579.

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Petz, Lawrence N. Expression of the Estrogen-Regulated pS2 Gene in MCF-7 Human Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, sierpień 1998. http://dx.doi.org/10.21236/ada360028.

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Petz, Lawrenec N. Expression of the Estrogen-Regulated pS2 Gene in MCF-7 Human Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2000. http://dx.doi.org/10.21236/ada392813.

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Awayda, Mouhamed S. Regulation of Multidrug Resistance Phenotype and P-Glycoprotein Activity in MCF-7 Cells by the Epthelial Na+ Channel. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2003. http://dx.doi.org/10.21236/ada420779.

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Bowen, Donnell. Selectivity of Very High Dose Methotrexate in MCF-7 and Normal Cells Using a Priming and Non-Toxic 5-Fluorouracil Dose. Fort Belvoir, VA: Defense Technical Information Center, październik 1999. http://dx.doi.org/10.21236/ada381717.

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Bowen, Donnell. Selectivity of Very High Dose Methotrexate in Mcf-7 and Normal Cells Using a Priming and Non-Toxic 5-Fluorouracil Dose. Fort Belvoir, VA: Defense Technical Information Center, październik 1998. http://dx.doi.org/10.21236/adb248375.

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Melkoumian, Zaroui. Regulation of C-myc Gene Expression by Potassium Channel Blocker Quindine in MCF-7 Human Breast Cancer Cell Line. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2000. http://dx.doi.org/10.21236/ada384096.

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Liu, Wei, i Javdutt Vadgama. Characterization of the Mechanisms of IGF-I-Mediated Stress-Activated Protein Kinase Activation in Human Breast Cancer Cell MCF-7. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2000. http://dx.doi.org/10.21236/ada392429.

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