Effect of miRNA-210 on proliferation, migration and invasion of human breast cancer cells
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Abstract:
Objective:To investigate the expression of miRNA-210(miR-210) in breast cancer tissues and its effect on proliferation, migration and invasion of breast cancer MDA-MB-231 cells. Methods: Tissues of breast cancer patients were collected from Department of Medical Oncology, First Affiliated Hospital of Kunming Medical University during October 2011 to June 2012. The expressions of miR-210 were compared between breast cancer tissues and the para-carcinoma tissues of 20 patients, as well as between breast cancer MDA-MB-231 cells and normal breast MCF-10a cells by real-time PCR. miR-210 inhibitor was transfected into breast cancer MDA-MB-231 cells by LipofectamineTM 2000 and the transfection efficiency was examined under a fluorescence microscope. Cell proliferation was evaluated by MTT assay and soft-agar colony formation assay. The cell cycle and apoptosis were detected by flow cytometry assay. The cell migration and invasion abilities were detected by migration and invasion assay. Results: The expressions of miR-210 in breast cancer tissues and cells were both significantly higher than those in para-carcinoma tissues and normal breast cells (P<0.01). miR-210 inhibitor was successfully transfected into MDA-MB-231 cells with a high transfection efficiency of (88.29±2.98)%. The proliferation ability of MDA-MB-231 cells was decreased significantly after transfection of miR-210 inhibitor (P<0.05). The percentages of cells in G0/G1 phase (\[64.23±3.12\]% vs \[5553±0.96\]%, P<0.01\] and of the apoptotic cells (\[31.90±305\]% vs \[15.98±0.63\]%, P<0.01) were significantly increased. The migration (\[291.00±43.12\] vs \[137.38±8349\], P<0.01\] and invasion (\[131.63±32.01\] vs \[647.88±31.20\], P<0.01\] of MDA-MB-231 cells were significantly inhibited. Conclusion:miR-210 is over-expressed in breast cancer tissues and cells. The proliferation, migration and invasion of human breast cancer MDA-MB-231 cells are inhibited after the transfection of miR-210 inhibitor.
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Project supported by the Science and Technology Condition Platform Construction Foundation of Yunnan Province (No. 2007DA006), and the Graduate Students Innovation Foundation of Kunming Medical University (No. 2012N06)