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. 2017 Jan 30;6(1):e292. doi: 10.1038/oncsis.2016.91

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Copyright © 2017 The Author(s)

Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Egr-1 promotes HCC Cells resistance to IR by facilitating irradiation-induced autophagy. (a) Repression of Egr-1 attenuates IR-induced autophagy. Cells were infected with Ad-GFP or Ad-DN-Egr-1. Western blot examines the expression of p62 and LC3 after IR (8 Gy) treatment. (b, c) Overexpression Egr-1 restores cell apoptosis caused by inhibition of autophagy by 3-MA, CQ or Atg4B siRNA. Cells were infected by Ad-GFP or Ad-Egr-1, followed 3-MA (2 mM), CQ (30 μm) treatment (b) or siRNA (100 nM) transfection. (c) The expression of apoptotic markers C-caspase-3, Bax, Bcl-2 and autophagy markers Atg4B and LC3 were detected by western blot. (d) Overexpression of Egr-1 increases colony-formation ability of HCC cells. Photography and graph indicates colony numbers of each experimental group.