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Table 1 HIF signal pathways in tumor immune escape

From: Hypoxia-inducible factors: master regulators of hypoxic tumor immune escape

Targets/effectors Model Mechanisms of tumor immune escape Refs.
CD47 Human breast cell lines HIF1 regulates CD47 expression to promote evasion of phagocytosis [93]
VEGF Human primary breast cells HIF1A-induced VEGF correlates with PD-L1 expression [91]
PD-L1 Human prostatic carcinoma cells
Mouse B16-F10 melanoma
HIF1A upregulates PD-L1 expression in tumor cells causing T-cell apoptosis [47]
VSIR BALB/c mice
CT26 colon carcinoma cell line
Hypoxia-induced VISTA, by HIF1A binding to the VISTA promoter, suppresses T-cell activity [27]
MICs The PANC-1 cell line
Human pancreatic carcinoma cells
Hypoxia-induced MICs are shed from the tumors membrane to evade KLRK1-mediated immune surveillance [101]
CCL28 Human haptic cell lines
Hepatic cell lines
Mouse hepatic cancer cells
HIF1A-dependently upregulates hypoxia-induced CCL28 to activate Tregs proliferation [103]
IL-23 Human ccRCC tumor cells Tumor cells induce tumor-infiltrating macrophages to secrete IL-23 by activating HIF1A, thereby inhibiting the killing capability of the cytotoxic lymphocytes [28]
miR224 Human prostate cancer tissues HIF1A upregulates miR-224 expression to inhibit the NK cells function by NCR1/NKp46 signaling [105]
GAL3ST1 786-O, RCC4, HEK293A, HEK293T, NK-92 cells, primary kidney tissues HIF1A and HIF2A upregulate the GAL3ST1 levels as VHL loss or hypoxia, further GAL3ST1 regulates sulfatide expression to escape the NK-mediated cytotoxicity [106]
SCF Human ccRCC tumor cells HIF2A induces the SCF secretion thereby reducing immunosurveillance and impairing anti-tumor immunity [29]