Schizandrin A promotes apoptosis in prostate cancer by inducing ROS-mediated endoplasmic reticulum stress and JNK MAPK signaling activation

Abstract

Background

Prostate cancer (PCa) is the most common malignant tumor in males with limited therapies. Schizandrin A (SchA) is a biologically active lignan isolated from the fruit of Schisandra chinensis. This research aimed to evaluate the roles and mechanisms of SchA in the progression of PCa.

Methods

PCa cells (VCap and DU145) treated with or without SchA were subjected to MTT assays, colony formation assays, DCFH-DA assays, western blotting, TUNEL staining, and flow cytometry analyses of cell cycle, cell apoptosis, and JC-1. Tumor xenograft model was established in nude mice to assess the in vivo effect of SchA.

Results

SchA suppressed cell proliferation and induced cell cycle arrest at G2/M and apoptosis in PCa cells. Additionally, SchA enhanced ROS generation and endoplasmic reticulum stress and activated JNK signaling to induce PCa apoptosis. Furthermore, SchA suppressed tumor growth in vivo.

Conclusion

SchA induces cell cycle arrest and apoptosis in PCa cells by activating ROS-mediated ER stress and JNK MAPK signaling.