LAUSR

ABSTRACT 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. HIGHLIGHTSOverexpression of EVA1A suppresses GBM cell growth.EVA1A induces autophagy through the mTOR/RPS6KB1 pathway.EVA1A induces GBM cell apoptosis.EVA1A inhibits the development of GBM in vivo.