KAT3B acts as an oncogene in PCa by mediating the succinylation of c-Myc and promoting its stability

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BACKGROUND: As a form of protein modification, succinylation significantly impacts protein function and helps govern a range of signaling mechanisms. This study was designed to explore the role of KAT3B, functioning as a succinylase, in the context of prostate cancer (PCa). METHODS: The expression levels were assessed using quantitative real-time PCR, Western blot, and immunofluorescence staining. To investigate protein-protein interactions, immunoprecipitation assays were performed. The interaction between proteins were confirmed by Co-immunoprecipitation assay. The cell phenotype of PCa cells was analyzed by CCK-8, flow cytometry, and transwell assays. RESULTS: We found that KAT3B was over-expressed in PCa tumor tissues and cells. Downregulated KAT3B decreased the viability, migration, and invasion while accelerating the apoptosis of PCa cells. Mechanistically, KAT3B mediated the succinylation of c-Myc, meantime promoted the stability of c-Myc. c-Myc overexpression reversed the role of KAT3B in PCa cells. The in vivo study verified that KAT3B silencing inhibited the growth of PCa cancer tissues. CONCLUSION: Our research indicates that KAT3B was highly expressed in PCa. KAT3B silencing inhibited PCa cell growth and cancer tissues growth by decreasing the succinylation and expression of c-Myc. These findings potentially contribute to novel approaches in diagnosing and treating PCa.

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