Article Publish Status: FREE
Abstract Title:

Sinomenine inhibits proliferation, migration, invasion and promotes apoptosis of prostate cancer cells by regulation of miR-23a.

Abstract Source:

Biomed Pharmacother. 2019 Apr ;112:108592. Epub 2019 Feb 18. PMID: 30784907

Abstract Author(s):

Feng Xu, Qi Li, Zhiyu Wang, Xiangming Cao

Article Affiliation:

Feng Xu


Background Prostate cancer is an extremely common disease in males, and the mortality of prostate cancer has been rising year by year. Sinomenine has been reported to exhibit anti-tumor effect on various cancers, but the function of Sinomenine in prostate cancer remains unclear. The study aimed to explore the effect of Sinomenine on proliferation, apoptosis, migration and invasion in prostate cancer cells. Methods PC3 cells were stimulated by different concentrations of Sinomenine, then cell proliferation, migration, invasion and apoptosis were examined by CCK-8, BrdU, Transwell and flow cytometry, respectively. Subsequently, miR-23a mimic and miR-23a inhibitor were transfected into PC3 and LNCaP cells, cell proliferation, apoptosis, migration and invasion were reassessed in these transfected cells. The related factors of cell cycle, apoptosis, metastasis and PI3K/AKT and JAK/STAT signal pathways were measured by western blot. Results Sinomenine significantly suppressed cell proliferation, promoted apoptosis and inhibited migration and invasion, as well as down-regulated Cyclin D1, CDK4, Bcl-2, MMP-2, MMP-9, Vimentin protein levels and up-regulated p16 and Bax protein levels in PC3 cells. Additionally, Sinomenine decreased the expression level of miR-23a, and overexpression of miR-23a reversed the effects of Sinomenine on cell proliferation, apoptosis, migration and invasion in PC3 and LNCaP cells. Further, Sinomenine inactivated PI3K/AKT and JAK/STAT signal pathways by regulation of miR-23a. Conclusions The data suggested that Sinomenine could suppress cell proliferation, migration, invasion, and promote apoptosis of prostate cancer cells through regulation of miR-23a. These findings might provide a possible strategy for the clinical treatment of prostate cancer.

Study Type : In Vitro Study

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