FERMT1 contributes to the progression of prostate cancer through the p53 pathway

Abstract

Purpose Fermitin family member 1 (FERMT1) is associated with the progression of different types of cancer. However, its biological functions of FERMT1 in prostate cancer (PC) are unclear. In this study, we preliminarily investigated the roles of FERMT1 and the mechanism by which it regulates the progression of PC. Methods The expression level of FERMT1 in PC tissues and cells was evaluated by immunohistochemical staining and Western blotting (WB) assay, respectively. Celigo cell count, cell counting kit-8 (CCK-8), flow cytometry, wound healing, Transwell assays and a mouse xenograft model was performed to evaluate the roles of FERMT1 in PC in vitro and in vivo. The interaction between p53 and FERMT1 was further investigated through co-immunoprecipitation (Co-IP). Finally, cells were treated with pifithrin-α (PFT-α), a p53 inhibitor, to investigate the regulatory role of p53 in the FERMT1-mediated progression of PC. Results FERMT1 was found to be upregulated in PC tissues and cells. Knocking down FERMT1 inhibited proliferation, migration, and cell cycle progression, and induced apoptosis in DU145 and LNCaP cell lines. Deleting FERMT1 also suppressed tumor growth of PC xenografts in vivo. More importantly, FERMT1 was discovered to play a significant role in cellular functions via the p53 signaling pathway, and the effects of FERMT1 knockdown on PC cellular function could be attenuated by pifithrin-α, a p53-inhibitor. Conclusions These findings of this study indicated that FERMT1 silencing partially inhibited PC progression via the p53 signaling pathway. Thus, FERMT1 is a promising potential therapeutic target for treating PC.