ArticleJournal of advanced research2026
PRDM15 inhibits responses of Tissue-Resident memory T cells by activating PVR/TIGIT axis to mediate gastric cancer immunosuppression.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Translational advances in gastric cancer: integrating biomarkers, novel therapies, and microenvironment remodeling in 2025.Translational cancer research · 2026Review
- Spatial immune niches in gastric cancer immunotherapy resistance: mechanisms and translational implications.Frontiers in immunology · 2026Review
- The role of immune checkpoint molecules in cancers.Frontiers in immunology · 2025Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionGastric cancer (GC) has shown relatively poor responses to existing immune therapies. The extensive infiltration of tissue-resident memory T cells (T
objectivesWe found that the T
methodsThe immune status of GC was evaluated by quantifying T cell subsets in GC tissues through flow cytometry. The biological functions and molecular mechanisms by which the oncogenic factor PRDM15 mediates tumor immune evasion were investigated through the PVR/TIGIT axis using transcriptome sequencing, Chromatin immunoprecipitation (ChIP) assay and Co-immunoprecipitation assay. The therapeutic potential of PRDM15/PVR/TIGIT was analyzed using tumor-bearing models.
resultsWe confirmed that PRDM15 promotes the transcription of PVR which is the ligand of TIGIT in GC cells. Aberrantly high expression of PRDM15 in GC tissues was associated with higher TNM stages and T cell immunosuppressive state in GC patients. PRDM15 was found to upregulate the proliferation, invasion and migration of GC cells. When co-cultured with T
conclusionThis study demonstrated that PRDM15 in GC cells could recruits the histone methyltransferase complex PRMT5/Mep50/WDR5 to promote PVR transcription, thereby activating the PVR/TIGIT axis, which inhibits T
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