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. 2021 Jul 29;11:687871. doi: 10.3389/fonc.2021.687871

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Copyright © 2021 Yang, Jin, Dai, Shan, Chen, Cai, Yang, Tang and Li

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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Identification of phosphatidylinositol 3-kinase (PI3K)/Akt as an important downstream factor regulating vascular endothelial growth factor (VEGF) and glycogen synthase kinase (GSK)3/β-catenin in hepatocellular carcinoma (HCC) cells. (A) Gene Ontology (GO) biological process analysis of the 54 proteins enriched in the PI3K/Akt pathway. (B) The proteins in the PI3K/Akt signaling pathway with the most significant changes in phosphorylation (greater than 2-fold). (C) The changes in the phosphorylation of proteins involved in VEGF/vascular endothelial growth factor receptor (VEGFR) signaling, GSK3/β-catenin signaling, and apoptosis. The data of each phosphorylation site level exhibited were the mean of two biological replicates. (D) The fluorescence signal values, standard curves, and calculated concentrations of granulocyte-macrophage colony-stimulating factor (GM-CSF) and VEGF in mortalin-plasmid- and vector-transfected HepG2 cells in the angiogenic antibody array. Means and standard deviations were calculated from replicate samples, and the differences were analyzed using Student’s t-test. (E) An outline map speculating the potential mechanisms involved in mortalin-induced angiogenesis and sorafenib resistance.