Hypoxia‑inducible factors: master regulators of hypoxic tumor immune escape
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62690094%3A18470%2F22%3A50019193" target="_blank" >RIV/62690094:18470/22:50019193 - isvavai.cz</a>
Alternative codes found
RIV/00216305:26620/22:PU144963 RIV/62156489:43210/22:43921556
Result on the web
<a href="https://jhoonline.biomedcentral.com/articles/10.1186/s13045-022-01292-6" target="_blank" >https://jhoonline.biomedcentral.com/articles/10.1186/s13045-022-01292-6</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1186/s13045-022-01292-6" target="_blank" >10.1186/s13045-022-01292-6</a>
Alternative languages
Result language
angličtina
Original language name
Hypoxia‑inducible factors: master regulators of hypoxic tumor immune escape
Original language 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.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30205 - Hematology
Result continuities
Project
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Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2022
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Journal of Hematology and Oncology
ISSN
1756-8722
e-ISSN
1756-8722
Volume of the periodical
15
Issue of the periodical within the volume
1
Country of publishing house
GB - UNITED KINGDOM
Number of pages
18
Pages from-to
"Article Number: 77"
UT code for WoS article
000805824600001
EID of the result in the Scopus database
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