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. 2020 Oct 22;11(10):898. doi: 10.1038/s41419-020-03107-3

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© The Author(s) 2020

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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Fig. 5 — A The protein levels of ClC-3 and SGK1 were significantly increased in the two ClC-3 OV cells treated with 20 μM olaparib (n = 3). vector empty vector-transfected cells, ClC-3 ClC-3 overexpression cells, ClC-3+shNC ClC-3 overexpression and SGK1 negative control cells, ClC-3+ shSGK1 ClC-3 overexpression and SGK1 knockdown cells. B, C Up-regulation of ClC-3/SGK1 axis enhanced olaparib-induced cell clonogenicity inhibition, and the enhancement effect could be attenuated by SGK1 KD (n = 3). D, E Up-regulation of ClC-3/SGK1 axis enhanced olaparib-induced cell cycle arrest at the G0/G1 phase, and the enhancement effect could be attenuated by SGK1 KD (n = 3). * P < 0.05.