miR‑122 promotes proliferation and invasion of clear cell renal cell carcinoma by suppressing Forkhead box O3

miR-122 通过抑制 Forkhead box O3 促进透明细胞肾细胞癌的增殖和侵袭

阅读:5
作者:Wenyuan Nie, Dong Ni, Xin Ma, Yu Zhang, Yu Gao, Cheng Peng, Xu Zhang

Abstract

MicroRNAs (miRNAs) serve an important role in renal cancer, but renal cancer miRNA expression data remains inconsistent. Therefore, there is a requirement for integrated analysis of these data. An increasing number of studies demonstrate that miR‑122 is dysregulated in numerous cancer types, including liver, lung and breast cancer, yet its role in clear cell renal cell carcinoma (ccRCC) remains unclear. In the present study, an integrated analysis of four ccRCC miRNAs expression datasets was performed and the expression of miR‑122 in the present cohort was validated. The effects of cell proliferation, colony formation, migration and invasion of ccRCC cells in vitro were assayed following transfection with miR‑122 mimics and inhibitor. The target gene of miR‑122 was confirmed using a luciferase reporter assay, and a xenograft mouse model was used to determine the effect of miR‑122 in ccRCC tumorigenicity in vivo. The present results demonstrated that patients with ccRCC with an increased miR‑122 level in tumor tissues had a shortened metastasis‑free survival time as indicated by The Cancer Genome Atlas‑Kidney Renal Clear Cell Carcinoma dataset and the present ccRCC cohort. Overexpression of miR‑122 in 786‑O cells improved cell proliferation, colony formation, migration and invasion, while knockdown of miR‑122 in SN12‑PM6 cells inhibited cell growth, colony formation, migration and invasion. Western blot analysis and luciferase reporter assays were used to identify FOXO3 as a direct target of miR‑122. The present results indicate that miR‑122 serves a tumor‑promoting role by direct targeting FOXO3 in ccRCC.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。