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MicroRNA-203 通过抑制 Cav1 使 PI3K/AKT 信号通路失活，从而抑制肾透明细胞癌细胞的上皮-间充质转化、迁移和侵袭。

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.

机构信息

Department of Radiology, China-Japan Union Hospital of Jilin University , Changchun, P. R. China.

Department of Urology Surgery, China-Japan Union Hospital of Jilin University , Changchun, P. R. China.

出版信息

Cell Adh Migr. 2020 Dec;14(1):227-241. doi: 10.1080/19336918.2020.1827665.

DOI:10.1080/19336918.2020.1827665
PMID:32990143
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7714454/
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.

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，CAV1 上调。上调的 miR-203 和下调的 CAV1 增加了 E-钙黏蛋白的表达和细胞凋亡，降低了β-连环蛋白和 N-钙黏蛋白的表达和细胞增殖、迁移和侵袭，并阻止了细胞周期进入。CAV1 是 miR-203 的靶基因，上调的 miR-203 使其下调，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 通过直接抑制 CAV1 抑制了 RCC 细胞的 EMT，从而抑制了 PI3K/AKT 信号通路的激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/b7d7d9946f8c/KCAM_A_1827665_F0011_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/98a8348ae680/KCAM_A_1827665_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/709874e869a0/KCAM_A_1827665_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/177da59e11ea/KCAM_A_1827665_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/690eeceea1d3/KCAM_A_1827665_F0008_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/223a6390bd62/KCAM_A_1827665_F0009_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/b7d7d9946f8c/KCAM_A_1827665_F0011_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/29fff21aefe4/KCAM_A_1827665_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/8b8fa66ec4b6/KCAM_A_1827665_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/c06e20df3ff0/KCAM_A_1827665_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/e138e2d1a1e9/KCAM_A_1827665_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/98a8348ae680/KCAM_A_1827665_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/709874e869a0/KCAM_A_1827665_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/177da59e11ea/KCAM_A_1827665_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/690eeceea1d3/KCAM_A_1827665_F0008_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/223a6390bd62/KCAM_A_1827665_F0009_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09d6/7714454/b7d7d9946f8c/KCAM_A_1827665_F0011_OC.jpg

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