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. 2020 Apr 17;10:545. doi: 10.3389/fonc.2020.00545

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Copyright © 2020 Wencong, Jinghan, Yong, Jianyang, Bin, Qingbao, Chen and Xiaoqing.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Akt/mTOR signaling pathway was involved in FOXK1-mediated proliferation, migration and invasion of GBC cells. (A) The protein expression of Akt, p-Akt(Ser473), mTOR, and p-mTOR (Ser 2448)in indicated cells was examined by Western blotting. (B) CCK-8 assay showed that the AKT special inhibitor MK2206 could abolish the enhanced proliferation by FOXK1 overexpression. (C,D) Transwell migration and matrigel invasion assay showed that the increasing mobility of GBC cells induced by FOXK1 overexpression was abrogated by MK2206. The number of invaded cells were calculated and depicted in the bar chart. (E) MK2206 reversed effects of FOXK1 overexpression on the expression of phosphorylated Akt (Ser473) and mTOR (Ser 2448) by Western blotting (*P < 0.05, **P < 0.01, and ***P < 0.001).