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Title: EVA1A inhibits GBM cell proliferation by inducing autophagy and apoptosis

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. - Highlights: • Overexpression 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.

Authors:
; ;  [1];  [1];  [2];  [1];  [3];  [4];  [1]
  1. Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191 (China)
  2. (Singapore)
  3. Department of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191 (China)
  4. (China)
Publication Date:
OSTI Identifier:
22649828
Resource Type:
Journal Article
Resource Relation:
Journal Name: Experimental Cell Research; Journal Volume: 352; Journal Issue: 1; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ADENOVIRUS; APOPTOSIS; BUDR; CELL PROLIFERATION; DOSES; ENDOPLASMIC RETICULUM; GLIOMAS; IN VITRO; IN VIVO; INACTIVATION; INDUCTION; INHIBITION; LYSOSOMES; MICE; PHOSPHOTRANSFERASES; PLANT GROWTH; POLYPEPTIDES; REGULATIONS; TIME DEPENDENCE; TUMOR CELLS; VECTORS; VISIBLE RADIATION

Citation Formats

Shen, Xue, Kan, Shifeng, Liu, Zhen, Lu, Guang, Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Zhang, Xiaoyan, Chen, Yingyu, Peking University Center for Human Disease Genomics, Beijing 100191, and Bai, Yun, E-mail: baiyun@bjmu.edu.cn. EVA1A inhibits GBM cell proliferation by inducing autophagy and apoptosis. United States: N. p., 2017. Web. doi:10.1016/J.YEXCR.2017.02.003.
Shen, Xue, Kan, Shifeng, Liu, Zhen, Lu, Guang, Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Zhang, Xiaoyan, Chen, Yingyu, Peking University Center for Human Disease Genomics, Beijing 100191, & Bai, Yun, E-mail: baiyun@bjmu.edu.cn. EVA1A inhibits GBM cell proliferation by inducing autophagy and apoptosis. United States. doi:10.1016/J.YEXCR.2017.02.003.
Shen, Xue, Kan, Shifeng, Liu, Zhen, Lu, Guang, Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Zhang, Xiaoyan, Chen, Yingyu, Peking University Center for Human Disease Genomics, Beijing 100191, and Bai, Yun, E-mail: baiyun@bjmu.edu.cn. Wed . "EVA1A inhibits GBM cell proliferation by inducing autophagy and apoptosis". United States. doi:10.1016/J.YEXCR.2017.02.003.
@article{osti_22649828,
title = {EVA1A inhibits GBM cell proliferation by inducing autophagy and apoptosis},
author = {Shen, Xue and Kan, Shifeng and Liu, Zhen and Lu, Guang and Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597 and Zhang, Xiaoyan and Chen, Yingyu and Peking University Center for Human Disease Genomics, Beijing 100191 and Bai, Yun, E-mail: baiyun@bjmu.edu.cn},
abstractNote = {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. - Highlights: • Overexpression 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.},
doi = {10.1016/J.YEXCR.2017.02.003},
journal = {Experimental Cell Research},
number = 1,
volume = 352,
place = {United States},
year = {Wed Mar 01 00:00:00 EST 2017},
month = {Wed Mar 01 00:00:00 EST 2017}
}