| First Author | Shen X | Year | 2017 |
| Journal | Exp Cell Res | Volume | 352 |
| Issue | 1 | Pages | 130-138 |
| PubMed ID | 28185834 | Mgi Jnum | J:260998 |
| Mgi Id | MGI:6151756 | Doi | 10.1016/j.yexcr.2017.02.003 |
| Citation | Shen X, et al. (2017) EVA1A inhibits GBM cell proliferation by inducing autophagy and apoptosis. Exp Cell Res 352(1):130-138 |
| abstractText | Eva-1 homolog A (EVA1A) is a novel lysosome and endoplasmic reticulum-associated protein involved in autophagy and apoptosis. In this study, we constructed a recombinant adenovirus 5-EVA1A vector (Ad5-EVA1A) to overexpress EVA1A in glioblastoma (GBM) cell lines and evaluated its anti-tumor activities in vitro and in vivo. We found that overexpression of EVA1A in three GBM cell lines (U251, U87 and SHG44) resulted in a suppression of tumor cell growth via activation of autophagy and induction of cell apoptosis in a dose- and time-dependent manner. EVA1A-mediated autophagy was associated with inactivation of the mTOR/RPS6KB1 signaling pathway. Furthermore in vivo, overexpression of EVA1A successfully inhibited tumor growth in NOD/SCID mice. Our data suggest that EVA1A-induced autophagy and apoptosis play a role in suppressing the development of GBM and their up-regulation may be an effective method for treating this form of cancer. |
