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. 2020 Sep 30;39:204. doi: 10.1186/s13046-020-01709-5

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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. 3 — Schematic representation of key VEGF/VEGFR signal transduction pathways. Proliferation: VEGFR can interact with Grab/Src/Gab1/Shb/PKCγ to activate RAF/MEK/MAPK and PI3K/AKT signaling pathways, and promote the proliferation of endothelial cells. Migration and invasion: VEGFR can activate PI3K/AKT by binding to cdc42, Rho, and RacGTPases, and promotes the migration and invasion of endothelial cells. Permeability: VEGFR can enhance blood vessel permeability by activating NFAT/β-catenin/VE-cadherin, and eNOS. Vasculogenic mimicry: VEGFR can promote EMT-induced vasculogenic mimicry by upregulating the expression of EMT-related genes