ArticleScientific reports2026
RASIP1-positive TECs in pancreatic adenocarcinoma: a potential novel type of endothelial cells correlated with "hot" tumors.
Article in Scientific reports, 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
Pancreatic adenocarcinoma (PDAC) is a highly lethal malignancy characterized by profound resistance to immunotherapy. Converting immunologically “cold” tumors into “hot” tumors by enhancing T cell infiltration represents a promising therapeutic strategy, yet the vascular mechanisms regulating immune recruitment in PDAC remain poorly defined. Here, we integrated single-cell RNA sequencing with GEPIA analysis and spatial transcriptomics to investigate the functional role of Ras Interacting Protein 1 (RASIP1)-positive endothelial cells in PDAC. We identified RASIP1-positive tumor endothelial cells as a distinct endothelial subpopulation enriched in leukocyte transendothelial migration pathways, with upregulated adhesion molecules and spatial co-localization with T-effector and IFN-γ signatures. Multiplex immunohistochemistry of human PDAC tissues revealed prominent perivascular accumulation of CD8⁺/GranzymeB⁺ cytotoxic T lymphocytes surrounding RASIP1-positive vessels. Mechanistically, RASIP1 knockdown reduced ICAM1 expression, whereas RASIP1 overexpression enhanced ICAM1 signaling, and both modulated ERK phosphorylation dynamics, suggesting that RASIP1 regulates endothelial functionality through ERK-related signaling. Collectively, our findings identify a distinct endothelial state that actively shapes the immune microenvironment of PDAC. Targeting RASIP1-positive endothelial cells may represent a potential strategy to enhance tumor immunogenicity and improve responsiveness to immunotherapy.
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