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. 2015 Dec 21;4(12):e180. doi: 10.1038/oncsis.2015.37

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Copyright © 2015 Macmillan Publishers Limited

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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ETO inhibits ACT cell growth. (a–d) Treatment of ETO (10 μM) for 24 h induces DNA damage response. ETO-treated H295 cells were co-stained with DNA dye (DAPI) with antibodies against (a) phospho-Ser139 of H2AX (γ-H2AX) or (b) phospho-Ser15 of p53 (p-p53). CTL: control (DMSO) treatment. Extracts of ETO-treated H295 cells were analyzed with antibodies against (c) phospho-Ser139 of H2AX (γ-H2AX) and GAPDH, or (d) p53, phospho-Ser15 of p53 (p-p53) and Ku70. (e and f) ETO inhibits ACT cell growth. The numbers of ACT H295 (e) and Y1 (f) cells were quantified in scramble control (CTL) or ETO treatment at different concentrations for different time points. n.s., no significance, **P<0.01, ***P<0.001.