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MicroRNA-203 inhibits epithelial-mesenchymal transition, migration, and invasion of renal cell carcinoma cells via the inactivation of the PI3K/AKT signaling pathway by inhibiting CAV1
Cell Adhesion & Migration ( IF 3.2 ) Pub Date : 2020-11-22 , DOI: 10.1080/19336918.2020.1827665
Ning Han 1 , Hai Li 2 , Hui Wang 3
Affiliation  

ABSTRACT

The present study aimed to evaluate the underlying mechanism of microRNA-203 (miR-203) in renal cell carcinoma (RCC) involving the PI3K/AKT signaling pathway. The results revealed downregulated miR-203 and upregulated CAV1 in RCC tissues. Upregulated miR-203 and downregulated CAV1 increased E-cadherin expression and cell apoptosis, decreased β-catenin and N-cadherin expression and cell proliferation, migration and invasion, and blocked cell cycle entry. CAV1, a target gene of miR-203, decreased by up-regulated miR-203, and silencing CAV1 led to the inactivation of PI3K/AKT signaling pathway. In conclusion, our findings suggested that miR-203-mediated direct suppression of CAV1 inhibits EMT of RCC cells via inactivation of the PI3K/AKT signaling pathway.



中文翻译:

MicroRNA-203通过抑制CAV1使PI3K/AKT信号通路失活,从而抑制肾细胞癌细胞的上皮间质转化、迁移和侵袭

摘要

本研究旨在评估 microRNA-203 (miR-203) 在肾细胞癌 (RCC) 中涉及 PI3K/AKT 信号通路的潜在机制。结果显示RCC组织中miR-203下调和CAV1上调。上调 miR-203 和下调 CAV1 增加 E-cadherin 表达和细胞凋亡,降低 β-catenin 和 N-cadherin 表达和细胞增殖、迁移和侵袭,并阻止细胞周期进入。miR-203 的靶基因 CAV1 被上调的 miR-203 降低,沉默 CAV1 导致 PI3K/AKT 信号通路失活。总之,我们的研究结果表明,miR-203 介导的 CAV1 直接抑制通过 PI3K/AKT 信号通路的失活来抑制 RCC 细胞的 EMT。

更新日期:2020-11-23
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