miR-675-5p regulation of autophagy by TSC2 promotes cisplatin resistance in ovarian cancer.

miR-675-5p 通过 TSC2 调控自噬,促进卵巢癌对顺铂产生耐药性

阅读:8
作者:Yang Tao, Liu Yuan, Liu Hong, Zhang Hongjun, Zhao Yi, Luo Ande, He Minjie
Ovarian cancer (OC) is a type of gynecological cancer, characterized by a high mortality rate. MicroRNAs (miRNAs) and cell autophagy are associated with the chemoresistance of tumors. The purpose of this study was to investigate the role of miR-675-5p in cisplatin (DDP) resistance in OC cells and its related mechanism. We collected OC tissues and paracancerous tissues. The OC cell line A2780 and the DDP-resistant cell line A2780/DDP were used for the study. RT-qPCR, Western blot and immunofluorescence were used to detect the expression of related genes and proteins. Cell proliferation and apoptosis were evaluated by CCK-8 assay and flow cytometry. Furthermore, the effect of miR-675-5p on the progression of OC was investigated in a xenograft model of nude mice. In this research, miR-675-5p expression was significantly increased in OC tissues and A2780/DDP cells. The suppression of miR-675-5p in A2780/DDP cells resulted in a significant reduction in DDP resistance. Further study revealed that miR-675-5p inhibited TSC2 expression in OC cells by binding to the TSC2 3'UTR, thereby activating the mTOR signaling pathway and promoting autophagy in A2780/DDP cells. Knocking down miR-675-5p suppressed DDP resistance in A2780/DDP cells through TSC2/mTOR axis, while overexpressing miR-675-5p suppressed DDP sensitivity in A2780 cells through TSC2. The tumor volume was decreased after injection of miR-675-5p-knockdown A2780/DDP cells in vivo. Knocking down miR-675-5p can inhibit the mTOR signaling pathway and autophagy through TSC2, thereby reducing the DDP resistance of OC cells. This may provide a potential therapeutic target for OC.

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。