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. 2019 Jul 22;38:324. doi: 10.1186/s13046-019-1284-y

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 6 — PI3K/AKT signaling pathway plays an important role in HERG1-dependent TXNDC5 upregulation. a HERG1-overexpressing TE-1 cells and HERG1-knockdown KYSE-30 cells were analyzed by western blotting to assess the expression of HERG1 and accumulation of JNK1/2, p38, PI3K, AKT, and Src, as well as their phosphorylated forms (n = 3). (b and c) HERG1, TXNDC5, p21, cyclin D1, E-cadherin, vimentin, and fibronectin expression in TE-1 cells administered the PI3K/AKT inhibitor LY294002 for 24 h in the presence or absence of HERG1 overexpression according to qPCR (b) and western blot analyses (c). HERG1, TXNDC5, p21, cyclin D1, E-cadherin, vimentin, and fibronectin expression in KYSE-30 cells transfected with HERG1 shRNA and/or AKT cDNA according to qPCR (b) and western blot analyses (c) (n = 3)