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miR-135 regulated breast cancer proliferation and epithelial-mesenchymal transition acts by the Wnt/β-catenin signaling pathway

机译:miR-135通过Wnt /β-catenin信号通路调节乳腺癌的增殖和上皮-间质转化

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摘要

Breast cancer (BC) is the most common cancer in women around the world. microRNAs (miRNAs/miRs) have been proved to be associated with the development and progression of breast cancer. In the present study, to elucidate the effects of dysregulated miR-135 on cells and underlying mechanisms in BC, in vitro and in vivo experiments were conducted. The biological functions of miR-135 were studied using MTT, colony formation, wound healing, transwell assays as well as tumorigenicity analysis. Gain- and loss- of function of miR-135 studies revealed that ectopic expression of miR-135 in MDA-MB-468 and MCF-7 cells significantly inhibited cell growth, migration, invasion and EMT, at least in part through inhibiting the activation of the Wnt/β-catenin pathway. Moreover, this was reversed in cells which were transfected with miR-135 inhibitors. Taken together, the results of the present study provided evidence that miR-135 acted as a tumor suppressor in BC, which may represent a novel therapeutic strategy for the diagnosis and prognosis of BC.
机译:乳腺癌(BC)是全世界女性中最常见的癌症。 microRNA(miRNA / miRs)已被证明与乳腺癌的发生和发展有关。在本研究中,为阐明miR-135失调对BC细胞和基础机制的影响,进行了体外和体内实验。使用MTT,集落形成,伤口愈合,transwell分析以及致瘤性分析研究了miR-135的生物学功能。 miR-135功能的获得和丧失表明,miR-135在MDA-MB-468和MCF-7细胞中的异位表达显着抑制了细胞的生长,迁移,侵袭和EMT,至少部分是通过抑制激活Wnt /β-catenin途径此外,在用miR-135抑制剂转染的细胞中,这是相反的。综上所述,本研究的结果提供了证据,证明miR-135在BC中起着抑癌作用,这可能代表了BC诊断和预后的新治疗策略。

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