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Title:
Hypoxia-inducible factors: master regulators of hypoxic tumor immune escape | Journal of Hematology & Oncology
Description:
Hypoxia, a common feature of the tumor microenvironment in various types of cancers, weakens cytotoxic T cell function and causes recruitment of regulatory T cells, thereby reducing tumoral immunogenicity. Studies have demonstrated that hypoxia and hypoxia-inducible factors (HIFs) 1 and 2 alpha (HIF1A and HIF2A) are involved in tumor immune escape. Under hypoxia, activation of HIF1A induces a series of signaling events, including through programmed death receptor-1/programmed death ligand-1. Moreover, hypoxia triggers shedding of complex class I chain-associated molecules through nitric oxide signaling impairment to disrupt immune surveillance by natural killer cells. The HIF-1-galactose-3-O-sulfotransferase 1-sulfatide axis enhances tumor immune escape via increased tumor cell-platelet binding. HIF2A upregulates stem cell factor expression to recruit tumor-infiltrating mast cells and increase levels of cytokines interleukin-10 and transforming growth factor-β, resulting in an immunosuppressive tumor microenvironment. Additionally, HIF1A upregulates expression of tumor-associated long noncoding RNAs and suppresses immune cell function, enabling tumor immune escape. Overall, elucidating the underlying mechanisms by which HIFs promote evasion of tumor immune surveillance will allow for targeting HIF in tumor treatment. This review discusses the current knowledge of how hypoxia and HIFs facilitate tumor immune escape, with evidence to date implicating HIF1A as a molecular target in such immune escape. This review provides further insight into the mechanism of tumor immune escape, and strategies for tumor immunotherapy are suggested.
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Keywords {🔍}
tumor, pubmed, cells, immune, cancer, google, scholar, article, hifa, cas, cell, expression, escape, hypoxia, central, pdl, hypoxic, hif, promotes, growth, metastasis, hifs, signaling, resistance, microenvironment, tumors, carcinoma, wang, factor, induces, promote, stem, target, role, res, hypoxiainducible, mechanisms, gene, chen, lncrnas, zhang, factors, progression, angiogenesis, protein, conditions, emt, foxdas, evasion, mechanism,
Topics {✒️}
hif1-galactose-3-o-sulfotransferase 1 akt/mtor/hif-1 alpha axis regulating mir-185-5p/hmga2 axis nf-κb-interacting lncrna modulates atp-binding cassette subfamily hypoxia-/hif-1 alpha-driven factors pd-l1/pd-1 immune checkpoint hypoxia-inducible factors hif-1alpha pd-l1/pd-1 signaling reverses regulating pd-1/pd-l1 checkpoint mir-619-5p/camk1d axis hypoxia-induced pd-l1 expression hif-2α promotes conversion platelet-derived growth factor hif-induced foxd2-as1 vhl/hif pathway-driven cancers hypoxia-inducible factor-1α lncrna ilf3-as1 promotes hypoxia-inducible factor 1-alpha positive pd-l1 expression regulating lncrna foxd2-as1 pd-1/pd-l1 blockade upregulate small hairpin hif-1α von hippel-lindau high gal3st1-sulfatide expression hypoxia-inducible factor-1alpha hypoxia-driven immune escape alkbh5-mediated m6a-demethylation activation-induced cell death transforming growth factor-β sponging mir-27a-3p stem cell differentiation hypoxia enhanced mdsc-mediated tgf-α/egfr pathway [163] neoantigen-directed immune escape hypoxia-induced vista promotes mediating nf-κb activation pi3k/akt signal induced small-cell lung carcinoma tumor-infiltrating mast cells small-cell lung cancer tgf-β2 jointly activate article download pdf pd-d1/pd-l1 17-allyl-amino-geldanamycin inhibits hypoxia-mediated immune escape nk cell-mediated cytotoxicity zinc finger mynd-type hypoxia-mediated immune evasion pd-1/pd-l1 pathway
Questions {❓}
- Functional regulation of HIF-1α under normoxia–is there more than post-translational regulation?
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headline:Hypoxia-inducible factors: master regulators of hypoxic tumor immune escape
description:Hypoxia, a common feature of the tumor microenvironment in various types of cancers, weakens cytotoxic T cell function and causes recruitment of regulatory T cells, thereby reducing tumoral immunogenicity. Studies have demonstrated that hypoxia and hypoxia-inducible factors (HIFs) 1 and 2 alpha (HIF1A and HIF2A) are involved in tumor immune escape. Under hypoxia, activation of HIF1A induces a series of signaling events, including through programmed death receptor-1/programmed death ligand-1. Moreover, hypoxia triggers shedding of complex class I chain-associated molecules through nitric oxide signaling impairment to disrupt immune surveillance by natural killer cells. The HIF-1-galactose-3-O-sulfotransferase 1-sulfatide axis enhances tumor immune escape via increased tumor cell-platelet binding. HIF2A upregulates stem cell factor expression to recruit tumor-infiltrating mast cells and increase levels of cytokines interleukin-10 and transforming growth factor-β, resulting in an immunosuppressive tumor microenvironment. Additionally, HIF1A upregulates expression of tumor-associated long noncoding RNAs and suppresses immune cell function, enabling tumor immune escape. Overall, elucidating the underlying mechanisms by which HIFs promote evasion of tumor immune surveillance will allow for targeting HIF in tumor treatment. This review discusses the current knowledge of how hypoxia and HIFs facilitate tumor immune escape, with evidence to date implicating HIF1A as a molecular target in such immune escape. This review provides further insight into the mechanism of tumor immune escape, and strategies for tumor immunotherapy are suggested.
datePublished:2022-06-03T00:00:00Z
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Hypoxia
Hypoxia-inducible factors
Tumor disease
Immunotherapy
Personalized medicine
Oncology
Hematology
Cancer Research
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headline:Hypoxia-inducible factors: master regulators of hypoxic tumor immune escape
description:Hypoxia, a common feature of the tumor microenvironment in various types of cancers, weakens cytotoxic T cell function and causes recruitment of regulatory T cells, thereby reducing tumoral immunogenicity. Studies have demonstrated that hypoxia and hypoxia-inducible factors (HIFs) 1 and 2 alpha (HIF1A and HIF2A) are involved in tumor immune escape. Under hypoxia, activation of HIF1A induces a series of signaling events, including through programmed death receptor-1/programmed death ligand-1. Moreover, hypoxia triggers shedding of complex class I chain-associated molecules through nitric oxide signaling impairment to disrupt immune surveillance by natural killer cells. The HIF-1-galactose-3-O-sulfotransferase 1-sulfatide axis enhances tumor immune escape via increased tumor cell-platelet binding. HIF2A upregulates stem cell factor expression to recruit tumor-infiltrating mast cells and increase levels of cytokines interleukin-10 and transforming growth factor-β, resulting in an immunosuppressive tumor microenvironment. Additionally, HIF1A upregulates expression of tumor-associated long noncoding RNAs and suppresses immune cell function, enabling tumor immune escape. Overall, elucidating the underlying mechanisms by which HIFs promote evasion of tumor immune surveillance will allow for targeting HIF in tumor treatment. This review discusses the current knowledge of how hypoxia and HIFs facilitate tumor immune escape, with evidence to date implicating HIF1A as a molecular target in such immune escape. This review provides further insight into the mechanism of tumor immune escape, and strategies for tumor immunotherapy are suggested.
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Hypoxia
Hypoxia-inducible factors
Tumor disease
Immunotherapy
Personalized medicine
Oncology
Hematology
Cancer Research
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