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

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
Ning Han, Hai Li, Hui Wang
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引用次数: 9

摘要

本研究旨在探讨microRNA-203 (miR-203)在肾细胞癌(RCC)中参与PI3K/AKT信号通路的潜在机制。结果显示,在RCC组织中miR-203下调,CAV1上调。miR-203上调,CAV1下调,E-cadherin表达增加,细胞凋亡增加,β-catenin、N-cadherin表达减少,细胞增殖、迁移、侵袭减少,细胞周期进入受阻。miR-203的靶基因CAV1因miR-203上调而降低,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介导的直接抑制CAV1通过使PI3K/AKT信号通路失活来抑制RCC细胞的EMT。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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.

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.

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.

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.

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.

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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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