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目的探讨miR-34c对三阴性乳腺癌细胞增殖、侵袭的影响及可能的分子机制。方法利用化学合成的miR-34c mimics转染三阴性乳腺癌MDA-MB-231细胞,通过MTS实验、Transwell迁移实验观察过表达miR-34c后细胞增值及侵袭能力的变化;采用流式细胞术检测过表达miR-34c对细胞周期的影响;采用Western blot检测b-catenin及其下游靶蛋白的表达情况。结果 miR-34c过表达明显抑制MDA-MB-231细胞的增殖和侵袭。过表达miR-34c诱导细胞G1期阻滞。Western blot结果显示,过表达miR-34c的MDA-MB-231细胞b-catenin及其下游靶蛋白Cyclin D1、Snail、MMP2和MMP7的表达明显下调。过表达b-catenin则逆转miR-34c对MDA-MB-231细胞的增殖和侵袭的抑制作用。结论 miR-34c可能通过抑制b-catenin信号而抑制三阴性乳腺癌MDA-MB-231细胞增殖、侵袭。
Objective To investigate the effect of miR-34c on the proliferation and invasion of triple negative breast cancer cells and the possible molecular mechanisms. Methods The transfected triple-negative breast cancer MDA-MB-231 cells were transfected with chemically synthesized miR-34c mimics. The proliferation and invasiveness of miR-34c cells were observed by MTS assay and Transwell migration assay. Flow cytometry Overexpression of miR-34c on the cell cycle; Western blot detection of b-catenin and its downstream target protein expression. Results Overexpression of miR-34c significantly inhibited the proliferation and invasion of MDA-MB-231 cells. Overexpression of miR-34c induced cell arrest in G1 phase. Western blot results showed that the expression of b-catenin and its downstream target proteins Cyclin D1, Snail, MMP2 and MMP7 in MDA-MB-231 cells overexpressing miR-34c were significantly down-regulated. Overexpression of b-catenin reversed the inhibitory effect of miR-34c on the proliferation and invasion of MDA-MB-231 cells. Conclusion miR-34c may inhibit the proliferation and invasion of triple-negative breast cancer MDA-MB-231 cells by inhibiting b-catenin signaling.