PSMC2 serves as a potential regulatory target of EZH2 in promoting glioma progression via epithelial-mesenchymal transition.

Proteasome 26 S Subunit, ATPase 2 (PSMC2) was initially thought to be associated with the removal of misfolded or damaged proteins and the removal of excess proteins that are no longer necessary. However, recent studies have found that PSMC2 acts as an oncogene in the human body. In our research, PSMC2 serves as a tumor-initiating factor in glioma. Bioinformatics analysis of public databases, along with an examination of PSMC2 expression in glioma patients, revealed its high expression at both the mRNA and protein levels in this type of tumor. The expression of PSMC2 exhibits a negative correlation with glioma patient prognosis. Modulating PSMC2 levels through inhibition or overexpression alters glioma cell morphology and suppresses both proliferation and motility. Silencing PSMC2 impedes epithelial-mesenchymal transition (EMT), concurrently altering cellular polarity and cytoskeletal architecture. Mechanistically, proteomics analysis, corroborated by co-immunoprecipitation (CO-IP) and fluorescence co-localization assays, identified a interaction between PSMC2 and Enhancer of Zeste Homolog 2 (EZH2). Our research findings indicate that PSMC2 can promote the occurrence and development of glioma, and this process is closely related to EZH2. Targeting the PSMC2-EZH2 axis may become a promising option for glioma treatment.