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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. 8 — A Olaparib inhibited the PI3K/AKT pathway in STAD cells, and up-regulation of ClC-3/SGK1 axis enhanced olaparib-induced PI3K/AKT pathway inhibition (n = 3). vector, empty vector-transfected cells; ClC-3 ClC-3 overexpression cells. B Nude mice were subcutaneously injected with SGC-7901 cells, and representative images of STAD tumor xenografts were exhibited (n = 7 mice/group). C Down-regulation of ClC-3 attenuated olaparib-induced tumor weight reduction. D Down-regulation of ClC-3 attenuated olaparib-induced tumor volume decrease. E The expression of PCNA and MMP2 in tumor tissues was detected by IHC staining. F The proposed mechanism model of olaparib in STAD growth and migration. *P < 0.05.