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. 2017 Aug 2;7:7104. doi: 10.1038/s41598-017-07005-1

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© The Author(s) 2017

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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MI-res cells accumulate less cisplatin-induced DNA damage respect to parental cells. (A) Western blot analyses of S139 phosphorylated Histone H2AX (γH2AX) expression, used as marker of DNA damage, in parental and MI-res cells untreated (0) or treated with cisplatin for 16 and 24 hours, as indicated. Vinculin was used as loading control. (B) Dot blot analyses evaluating the amount of platinated-DNA in parental and MI-res cells untreated (NT) or treated with cisplatin for 16 and 24 hours and then released in cisplatin-free medium for additional 24 (+24) or 48 (+48) hours to allow for DNA repair. (C) FACS analyses of DNA content in TOV-112D parental and MI-res cells untreated (NT) or treated with cisplatin for 16 and 24 hours and then released in cisplatin-free medium for additional 4, 8 or 24 hours, as indicated. A typical histogram for each cell line is shown and the correspondent cell cycle distribution (mean ± SD n = 3 biological replicates) is reported in the lower tables.