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. 2020 Jul 6;39:128. doi: 10.1186/s13046-020-01638-3

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — NCSTN regulates β-catenin through Notch/AKT/GSK-3β signaling pathway. a The expression of N1ICD, N2ICD, N3ICD, and N4ICD in the indicated HCCLM3 and Hep3B cells. b Representative immunoblot analyses of total AKT, phosphorylated AKT (Ser473), GSK-3β, phosphorylated GSK-3β (ser9), β-catenin and phosphorylated β-catenin (Ser33/37/Thr41) in the indicated HCC cells. c The expression of N1ICD, AKT and p-AKT in the indicated Hep3B cells, treated with FLI-06 (the Notch inhibitor, 5 μM, 24 h). d Representative immunoblot analyses of AKT, p-AKT (Ser473), GSK-3β, p-GSK-3β (ser9), β-catenin and p-β-catenin (Ser33/37/Thr41) in the indicated Hep3B cells, treated with MK-2206 2HCl (the AKT inhibitor, 10 μM, 24 h). e Co-IP assays showed NCSTN regulated the interaction between GSK-3β and β-catenin in the indicated cells. f Immunofluorescence assays showed NCSTN-mediated nuclear translocation of β-catenin was rescued in cells treated with MK-2206 2HCl. g CCK8 assays showed that NCSTN-mediated cell growth could be rescued in Hep3B cells treated with MK-2206 2HCl. h, i The migration and invasion capacity was rescued in cells treated with MK-2206 2HCl. j The propose model showing the regulatory landscape of NCSTN/Notch/AKT/β-catenin signaling axis in promoting cell growth and metastasis of HCC. Loading control was evaluated by β-actin. *p < 0.05, **p < 0.01, ***p < 0.001