Altered expression of tumor protein D52 regulates apoptosis and migration of prostate cancer cells.

摘要: Tumor protein D52 (TPD52) is a found to be overexpressed in prostate and breast cancer due gene amplification. However, its physiological function remains under investigation. In the present study, we investigated response of LNCaP human carcinoma cell line deregulation TPD52 expression. Proteomic analysis biopsies showed overexpression at level, whereas transcriptional upregulation was demonstrated by real-time PCR. Transfection cells with specific small hairpin RNA giving efficient knockdown resulted significant death cells. As activation caspases (caspase-3 -9), loss mitochondrial membrane potential, occurs apoptosis. The disruption potential indicates that acts upstream apoptotic reaction. To study effect expression on proliferation, were either transfected enhanced green fluorescence protein-TPD52 or RNA. Enhanced overexpressing an increased proliferation rate, TPD52-depleted reverse effect. Additionally, demonstrate exogenous promotes migration via alphav beta3 integrin through kinase B/Akt signaling pathway. From these results, conclude plays important role various molecular events, particularly morphological diversification dissemination cells, may promising target respect developing new therapeutic strategies treat cancer.