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. 2017 Oct 9;7:12876. doi: 10.1038/s41598-017-13232-3

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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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PARP1 inhibition sensitizes CC cells and leads to rapid induction of DNA damage and cell death. (A) Bar graph showing the percentage of γH2A.X foci positive cells (cell with >20 positive foci/cell as compared to isotype) in indicated groups at particular treatment duration. At least 200 cells were counted in blind fashion in independent duplicate experiment. Error bar show SD from the mean of two independent counts. *p = 0.05, **p < 0.01, ***p < 0.001 (upper panel); Bar graph showing the percentage of γH2A.X foci positive cells in PARP1 silenced and control counterpart cells treated with 5 µM cisplatin for indicated time points. At least 200 cells were counted in blind fashion in independent duplicate experiment. Error bar display SD from the mean of two independent counts. *p = 0.05, **p < 0.01, ***p < 0.001 (lower panel). (B) Cell proliferation assay displaying effect of cisplatin on PARP1 silenced CC cells. (C) PARP1 silenced cells showing increased loss of clonogenic survival after cisplatin treatment in CC cells.