ArticleiScience2026
Hypoxic-immune axis orchestrates metastatic dissemination via HIF isoform imbalance in pancreatic neuroendocrine tumors.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Metastatic dissemination underpins mortality in pancreatic neuroendocrine tumors (PNETs), where the hypoxic, immunosuppressive microenvironment facilitates progression. Non-genetic determinants, including hypoxia-inducible factor (HIF) isoforms, preceding metastatic traits can disrupt immune homeostasis and promote aggression. However, the dynamics of HIF-immune crosstalk in PNET metastasis remain elusive. Using multi-omics and organoid models of KRAS-mutated PNETs, we uncovered rapid HIF isoform shifts, with HIF-1α/β overexpression and HIF-2α suppression emerging as pivotal. This imbalance is pronounced in advanced and metastatic PNETs. The hypoxic-immune axis is swiftly activated under pseudohypoxia and sustains in disseminated cells. It fuels immune evasion and invasion by enriching immunosuppressive cells and altering checkpoint signaling, interacting with KRAS-driven succinate accumulation. We propose that HIF isoform imbalance arises early in PNET evolution and orchestrates metastatic dissemination.
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