Abstract
Prostate cancer (PCa) is the second most common cancer in men worldwide, and understanding its molecular mechanisms is crucial for developing effective treatment strategies. SIRT7, a NAD+-dependent histone deacetylase, has emerged as a key regulator in PCa progression due to its roles in chromatin remodeling, DNA repair, and transcriptional regulation. Analysis of 492 PCa samples from The Cancer Genome Atlas (TCGA) via cBioPortal revealed that high SIRT7 expression is associated with poor prognosis in PCa patients. Mechanistically, SIRT7 deacetylates histone H3 at lysine 18 (H3K18Ac), a marker associated with aggressive tumors, suppressing tumor suppressor genes and promoting cancer cell proliferation and survival. Epithelial-mesenchymal transition (EMT) is a cellular biological process in which epithelial cells undergo specific molecular and morphological changes to transform into cells with characteristics of mesenchymal cells. SIRT7 also regulates EMT, and inhibiting SIRT7 in PCa cell lines reduces cell migration and invasion, highlighting its potential as a therapeutic target. In summary, the clinical significance of SIRT7 expression in PCa requires further research to elucidate its mechanisms. Developing specific inhibitors targeting SIRT7's deacetylase activity is a promising therapeutic strategy. SIRT7 plays a crucial role in regulating biological processes such as cell proliferation, cell cycle, and apoptosis in PCa through its epigenetic control of gene expression and maintenance of genomic stability. Therefore, SIRT7 may be a potential therapeutic target for PCa, and its expression could have prognostic value for PCa patients, providing important guidance for clinical monitoring and diagnosis by physicians.