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. Author manuscript; available in PMC: 2021 Oct 10.
Published in final edited form as: Cancer Lett. 2020 Jun 20;490:124–142. doi: 10.1016/j.canlet.2020.05.030

Figure 1: A schematic representation of hypoxia signaling cascades modulated by hypoxia inducible factors (HIFs) in tumor cells.

Figure 1:

HIFs promote metabolic adaptations, oxidative strees, angiogenesis, stromal cell recruitment, extracellular matrix modelling, extravasation, metastasis, migration and drug resistance through different signaling pathways. ATP-binding cassette subfamily G member 2 (ABCG2), AKT serine/threonine protein kinase B (AKT), Angiopoietin-1 (Ang-1), Angiopoietin-2 (Ang-2), B-cell lymphoma 2 (Bcl-2), Carbonic anhydrase IX (CAIX), Cyclooxygenase-2 (COX-2), C-X-C motif chemokine 4 (CXCR4), E-cadherin (E-cad), Forkhead box O3 (FOXO3A), Fibroblast growth factor (FGF), Glucose transporter 1 (GLUT-1), Lysyl oxidase (LOX), Inhibitor of apoptosis (IAP), Interleukin-6 (IL-6), Mitogen activated protein kinase (MAPK), Phospholipase C-gamma (PLC-γ), Monocarboxylate transporter 4 (MCT-4), Macrophage inhibitory cytokine-1 (MIC-1), Matrix metalloproteinases (MMPs), Mammalian target of rapamycin (mTOR), Nuclear factor kappa light chain enhancer of activated B cells (NF-κB), Platelet derived growth factor (PDGF), Phosphoglycerate kinase 1 (PGK1), Phosphatidylinositol 3-kinase (PI3K), Pyruvate kinase (PKM), Receptor tyrosine kinase (RTK), Stromal cell-derived factor 1 (SDF-1), Vascular endothelial growth factor (VEGF), Vascular endothelial growth factor receptor 1 (VEGFR1), Vascular endothelial growth factor receptor 2 (VEGFR2), von Hippel-Lindau tumor suppressor (VHL).