TSGA10, a new player in regulating autophagy and apoptosis

Abstract

Testis specific gene antigen 10 (TSGA10) overexpression could inhibit angiogenesis and tumor cell proliferation, migration and invasion through inhibiting HIF-1α. The exact role of TSGA10 in autophagy and apoptosis is not clear. Present study was conducted to investigate the potential effects of TSGA10 overexpression on regulation of autophagy and apoptosis. To do so, TSGA10-containing vector (pcDNA3.1-TSGA10 vector) was designed for stable and transient transfections in HeLa cells, and clonal selection was applied. Expression of autophagy and apoptosis-related genes was assessed by real-time RT-PCR in TSGA10-overexpressing cells compared with HeLa cells transfected by empty vector. Rate of autophagy and cell viability were assessed by acridine orange and MTT assays, respectively. Our findings showed that overexpression of TSGA10 would induce autophagy under normoxic and hypoxic conditions in the presence or absence of autophagy inducers. Expression levels of autophagy and apoptosis-related genes increased significantly in TSGA10-overexpressing cells compared with control cells. In addition, HeLa cells overexpressing TSGA-10 exhibited lower expression of BCL-2 and survival rates in comparison with control cells. Molecular docking results showed that interaction between TSGA10 and BCL-2 could inhibit anti-apoptotic activity of BCL-2. According to our findings, TSGA10 overexpression has a main role in regulating autophagy and apoptosis through inhibition of BCL-2. Therefore, TSGA10 could be considered as a new regulator of autophagy and apoptosis in future studies.