Multiple studies have confirmed the pro-oncogenic effects of PAX3 in an array of cancers, but its role in prostatic cancer (PCa) remains largely undefined. The aim of this study was to investigate the role of PAX3 in PCa. PAX3 expression was compared between PCa tumor tissue and non-tumor tissues and PCa cell lines and normal prostate epithelial cells (PNT2) by western blot analysis and immunohistochemistry (IHC) staining. MTT and immunofluorescence (IF) assays were used to detect PCa cell proliferation. Flow cytometry was used to evaluate cell apoptosis in PCa. Transwell assays were used for the determination of cell migration and PCa cell invasion. PAX3 expression was higher in PCa tissues and human PCa cell lines. Moreover, PAX3 silencing inhibited the proliferation, metastasis, and epithelial-mesenchymal transition (EMT) of PCa cells, and increased the rates of apoptosis. PAX3 silencing inhibited TGF-β/Smad signaling in PCa cells. The effects of si-PAX3 on the proliferation, apoptosis, metastasis and EMT of PCa cells were alleviated by TGF-β1 treatment. PAX3 silencing inhibits PCa progression through the inhibition of TGF-β/Smad signaling. This reveals PAX3 as a novel biomarker and therapeutic target for future PCa treatments. This article is protected by copyright. All rights reserved.
Cell biology international. 2020 Jul 16 [Epub ahead of print]
Ke Zeng, Wenxian Xie, Jun Huang, Jian Yang, Kefei Deng, Xiaohui Luo
Department of Urology, Zigong First People's Hospital, Zigong City, Sichuan, 643000, China., Department of Basic Medicine, Sichuan Vocational College of Health and Rehabilitation, Zigong City, Sichuan, 643000, China., Department of Urology, Baoji Central Hospital, Baoji City, Shaanxi, 721008, China.