کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10914709 | 1088807 | 2015 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The miR-200 family differentially regulates sensitivity to paclitaxel and carboplatin in human ovarian carcinoma OVCAR-3 and MES-OV cells
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کلمات کلیدی
RT-qPCRmiRNA or miRstearoyl-CoA desaturase-1MTHFD2TUBB3ALDH1A3HGSOCEpCAMNrf2SCDRRM2COL5A1COL6A1FACSCdh6methylenetetrahydrofolate dehydrogenaseepithelial mesenchymal transition - انتقال مزانشیمی epithelialepithelial to mesenchymal transition - اپیتلیال به انتقال مزانشیمالEMT - تکنسین فوریتهای پزشکیfluorescence-activated cell sorting - دسته بندی سلول های فعال فلورسنسreal time quantitative polymerase chain reaction - زمان واقعی واکنش زنجیره ای پلیمراز کمیHigh Grade Serous Ovarian Cancer - سرطان تخمدان سروز بالاmesenchymal to epithelial transition - مزانشیمی به انتقال اپیتلیالDrug resistance - مقاومت داروییMET - ملاقات کردepithelial cell adhesion molecule - مولکول چسبندگی سلولی اپیتلیالMicroRNA - میکرو RNA Paclitaxel - پاکلی تاکسلvascular cell adhesion protein 1 - پروتئین چسبندگی سلولی عروقی 1Carboplatin - کربوپلاتین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
We studied the role of miRNA-200 family members in cellular sensitivity to paclitaxel and carboplatin, using two ovarian cancer cell lines, OVCAR-3 and MES-OV, and their paclitaxel resistant variants OVCAR-3/TP and MES-OV/TP. Both resistant variants display a strong epithelial-mesenchymal transition (EMT) phenotype, with marked decreases in expression of miR-200c and miR-141 in OVCAR-3/TP, and down-regulation of all five members of the miR-200 family in MES-OV/TP. Lentiviral transfection of inhibitors of miR-200c or miR-141 in parental OVCAR-3 triggered EMT and rendered the cells resistant to paclitaxel and carboplatin. Conversely, the infection of OVCAR-3/TP cells with retroviral particles carrying the miR-200ab429 and 200c141 clusters triggered a partial mesenchymal to epithelial transition (MET). This partial MET was not sufficient to re-sensitize OVCAR-3/TP cells to paclitaxel. However, the miR-200c/miR-141 cluster transfectants became 6-8x resistant to carboplatin, an unexpected result, whereas miR-200a/miR-200b/miR-429 had no effect. Transfecting the OVCAR-3/TP GFP cells with specific miRNA mimics confirmed these data. MiR-200c and miR-141 mimics conferred resistance to carboplatin in MES-OV/TP cells, similar to OVCAR-3/TP, but sensitized MES-OV to paclitaxel. Several genes involved in balancing oxidative stress were altered in OVCAR-3/TP 200c141 cells compared to controls. The miR-200 family plays major, cell-context dependent roles in regulating EMT and sensitivity to carboplatin and paclitaxel in OVCAR-3 and MES-OV cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Oncology - Volume 9, Issue 8, October 2015, Pages 1678-1693
Journal: Molecular Oncology - Volume 9, Issue 8, October 2015, Pages 1678-1693
نویسندگان
Anamaria Brozovic, George E. Duran, Yan C. Wang, E. Brian Francisco, Branimir I. Sikic,