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. 2020 Aug 18;11(8):644. doi: 10.1038/s41419-020-02906-y

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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 NE phosphorylates the Ser473 and Thr308 residues of AKT in ovarian cancer cells by using western blotting at 24 h. b CCK-8 assay was used to evaluate the effects of different concentration of AKT inhibitor AKTi VIII on the viability of ovarian cancer cells at 24 h. c Western blotting showed that AKTi VIII inhibited NE-mediated activation of the AKT/β-catenin/SLUG axis in ovarian cells at 24 h. AKTi VIII reduces NE-mediated pro-migration (d) and pro-invasion (e) influence on ovarian cancer cells at 24 h. **P < 0.01; ***P < 0.001. Scale bar, 200 μM.