PAX3 silencing inhibits prostate cancer progression through the suppression of the TGF-β/Smad signaling axis.

Abstract

Multiple studies have confirmed the pro-oncogenic effects of PAX3 in an array of cancers, but its role in prostate cancer (PCa) remains largely undefined. The aim of this study is to investigate the role of PAX3 in PCa. PAX3 expression was compared between PCa tumor tissue and nontumor tissues and PCa cell lines and normal prostate epithelial cells (PNT2) by western blot analysis and immunohistochemistry staining. MTT and immunofluorescence 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 transforming growth factor-β (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.