Pathology, research and practice · 2025
Schizandrin A promotes apoptosis in prostate cancer by inducing ROS-mediated endoplasmic reticulum stress and JNK MAPK signaling activation.
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Peng Chang-Wei, Ma Pei-Li, Dai Hai-Tao
Аннотация
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.
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.