ArticleProceedings of the National Academy of Sciences of the United States of America2024
Deficiency of factor-inhibiting HIF creates a tumor-promoting immune microenvironment.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Unraveling the role of HIF-1 in peripheral blood mononuclear cells from older patients with Alzheimer's disease.Frontiers in aging neuroscience · 2026Article
- Tackling tumor hypoxia: advances in breaking the oncogenic HIF-1α-p300/CBP alliance.Investigational new drugs · 2025Review
- Research progress of CD73-adenosine signaling regulating hepatocellular carcinoma through tumor microenvironment.Journal of experimental & clinical cancer research : CR · 2025Review
- Cascade-recharged macrophage-biomimetic ruthenium-based nanobattery for enhanced photodynamic-induced immunotherapy.Journal of nanobiotechnology · 2025Article
- The role of mesenchymal stem cells in cancer and prospects for their use in cancer therapeutics.MedComm · 2024Review
- Deficiency of factor-inhibiting HIF creates a tumor-promoting immune microenvironment.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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Authors and funding
27 authors at 8 institutions in 5 countries.
Funding
Abstract
Hypoxia signaling influences tumor development through both cell-intrinsic and -extrinsic pathways. Inhibiting hypoxia-inducible factor (HIF) function has recently been approved as a cancer treatment strategy. Hence, it is important to understand how regulators of HIF may affect tumor growth under physiological conditions. Here we report that in aging mice factor-inhibiting HIF (FIH), one of the most studied negative regulators of HIF, is a haploinsufficient suppressor of spontaneous B cell lymphomas, particular pulmonary B cell lymphomas. FIH deficiency alters immune composition in aged mice and creates a tumor-supportive immune environment demonstrated in syngeneic mouse tumor models. Mechanistically, FIH-defective myeloid cells acquire tumor-supportive properties in response to signals secreted by cancer cells or produced in the tumor microenvironment with enhanced arginase expression and cytokine-directed migration. Together, these data demonstrate that under physiological conditions, FIH plays a key role in maintaining immune homeostasis and can suppress tumorigenesis through a cell-extrinsic pathway.
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