OGT-mediated O-GlcNAcylation of OR51F2 protein aggravates the malignant phenotypes of prostate cancer cells.

Prostate cancer (PCa) is the most prevalent male malignancies globally, and its incidence and mortality rates are constantly rising. The current study focuses on the novel molecular mechanism affecting PCa progression. Through analyzing the GSE246282 dataset, OR51F2 was selected as the research target because it presented the most significantly upregulation in PCa tissues. Moreover, OR51F2 expression was detected and found to be high in PCa cells at both mRNA and protein levels. Functionally, PCa cell proliferation and migration were repressed efficiently by silencing of OR51F2 expression. Mechanistically, OR51F2 protein was stabilized by OGT-induced O-GlcNAcylation. Furthermore, OGT overexpression led to the recovery of OGT silencing-induced suppression of PCa cell proliferation and migration. Dysregulation of signaling pathways contributes to tumorigenesis and cancer progression. Here, we determined that OGT and OR51F2 could activate Wnt/β-catenin signaling pathway. Finally, activation of Wnt pathway by LiCl treatment recovered the proliferation and migration of PCa cells repressed by OGT silencing. In conclusion, the present study indicated that OGT-induced O-GlcNAcylation of OR51F2 accelerated PCa progression via activating the Wnt/β-catenin pathway.