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. 2019 Sep 10;9:13045. doi: 10.1038/s41598-019-49631-x

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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ROS/JNK pathway mediates APE-induced cell cycle arrest, apoptosis, and autophagy in MDA-MB-231 cells. MDA-MB-231 cells were treated with APE 300 μM EqC with or without pretreatment with 5 mM NAC or 5 µM SP600125 for 1 h. (a) After 24 h the distribution of cell cycle was assessed by flow cytometry and the expression of cell cycle-related proteins was measured by western blotting. (b) After 24 h cell apoptosis was evaluated by flow cytometry and the expression of apoptosis-related proteins was measured by western blotting. (c) After 48 h autophagy was analyzed by flow cytometry and the levels of beclin-1, LC3B and p62 were analyzed by western blotting. All results were obtained from at least three independent experiments (*P < 0.05 versus control cells). The full-length blots are included in the supplementary information (Figs S8–S11).