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. 2018 Mar 2;8:3947. doi: 10.1038/s41598-018-22289-7

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© The Author(s) 2018

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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PTEN depletion diminishes DSB repair via homologous recombination. (A) yH2AX foci (red) at the indicated times after 2 Gy in mock- (siCTR) or PTEN-depleted DU145 cell nuclei (blue). (B) PTEN was efficiently depleted (insert) in HeLa cells harboring single copies of the HR-substrate pGC. After 24 h, cells were transfected with I-SceI expressing vector to induce DSB and the percentage of GFP-positive (GFP⁺) cells was measured using flow cytometry as an indicator of HR efficiency. (C–D) Survival fractions after treatment with the indicated concentrations of mitomycin C (C) or the PARP inhibitor olaparib (D) were measured in mock- (siCTR) or PTEN- depleted DU145 cells (siPTEN) using the colony forming assay. RAD51 was depleted using siRNA (siRAD51) as a positive control in all experiments. Shown are means ± SEM of three independent experiments. Asterisk (*) represents significant difference (P < 0.05).