MYO6 knockdown inhibits the growth and induces the apoptosis of prostate cancer cells by decreasing the phosphorylation of ERK1/2 and PRAS40

MYO6 敲低通过降低 ERK1/2 和 PRAS40 的磷酸化抑制前列腺癌细胞的生长并诱导其凋亡

阅读:11
作者:Dong Wang, Libing Zhu, Min Liao, Tengyue Zeng, Wenli Zhuo, Shunliang Yang, Weizhen Wu

Abstract

Prostate cancer is the second most frequently diagnosed cancer among males around the world. Myosin VI (MYO6), as a motor protein, has been reported to be implicated in cancer-related cell migration and cellular functions. To investigate the role of MYO6 in prostate cancer, immunohistochemical analysis was firstly applied to prostate cancer tissues and revealed that MYO6 was closely related with the Gleason score in prostate cancer. Then we used specific short hairpin RNA (shRNA) to downregulate MYO6 expression in DU145 and PC-3 cells and found that decreased MYO6 expression significantly suppressed cell proliferation, as determined by MTT and colony formation assays. Flow cytometry confirmed that the suppression of MYO6 promoted cell cycle arrest at the G2/M and sub-G1 phase in the DU145 cells. Furthermore, PathScan intracellular signaling array analysis demonstrated that the phosphorylation of ERK1/2 and PRAS40 was downregulated in the DU145 cells following MYO6 knockdown. Knockdown of MYO6 downregulated the expression of AKT3 and upregulated the expression of PARP, as confirmed by western blot analysis. These results suggest that MYO6 plays an essential role in the progression of prostate cancer and silencing of MYO6 may be a promising therapeutic approach for prostate cancer.

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。