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. 2019 Dec 10;8(12):1602. doi: 10.3390/cells8121602

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Hypoxia mediates pro-metastatic risk of vessel targeting agents. Hypoxia mediated by vessel targeting agents facilitates tumor epithelial mesenchymal transition (EMT) with decreased expression of epithelial cell markers and enhanced mesenchymal cell markers via the Wnt/β-catenin, transforming growth factor β (TGFβ) and HIV-1 Tat interactive protein 2 (HTATIP2) signaling pathways. Hypoxia contributes to tumor metabolism shift with increased glycolytic metabolism and lipid metabolism by upregulating fatty acid binding protein (FABP3), FABP7 and fatty acid synthase (FASN). Hypoxia also promotes the infiltration of bone marrow derived cells (BMDCs), including tumor associated macrophages (TAMs) and CD11b⁺ cells through colony-stimulating factor-1 (CSF-1), stromal-derived factor-1α (SDF-1α) and VEGF.