{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Passang T"],"funding":["Abraham J. and Phyllis Katz Foundation (Katz Foundation)","Abraham J. and Phyllis Katz Foundation","NCI NIH HHS"],"pagination":["2954-2967"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11458156"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["84(18)"],"pubmed_abstract":["Pancreatic ductal adenocarcinoma (PDAC) harbors a complex tumor microenvironment, and cross-talk among cells in the tumor microenvironment can contribute to drug resistance and relapse. Vasoactive intestinal peptide (VIP) is overexpressed in PDAC, and VIP receptors expressed on T cells are a targetable pathway that sensitizes PDAC to immunotherapy. In this study, we showed that pancreatic cancer cells engage in autocrine VIP signaling through VIP receptor 2 (VPAC2). High coexpression of VIP with VPAC2 correlated with reduced relapse-free survival in patients with PDAC. VPAC2 activation in PDAC cells upregulated Piwi-like RNA-mediated gene silencing 2, which stimulated cancer cell clonogenic growth. In addition, VPAC2 signaling increased expression of TGFβ1 to inhibit T-cell function. Loss "],"journal":["Cancer research"],"pubmed_title":["VPAC2 Receptor Signaling Promotes Growth and Immunosuppression in Pancreatic Cancer."],"pmcid":["PMC11458156"],"funding_grant_id":["R01 CA287866"],"pubmed_authors":["Liu Y","Passang T","Wang S","Zhang H","Ravindranathan S","Li JM","Wang W","Zeng F","Waller EK","Hsu PC","Lesinski GB"],"additional_accession":[]},"is_claimable":false,"name":"VPAC2 Receptor Signaling Promotes Growth and Immunosuppression in Pancreatic Cancer.","description":"Pancreatic ductal adenocarcinoma (PDAC) harbors a complex tumor microenvironment, and cross-talk among cells in the tumor microenvironment can contribute to drug resistance and relapse. Vasoactive intestinal peptide (VIP) is overexpressed in PDAC, and VIP receptors expressed on T cells are a targetable pathway that sensitizes PDAC to immunotherapy. In this study, we showed that pancreatic cancer cells engage in autocrine VIP signaling through VIP receptor 2 (VPAC2). High coexpression of VIP with VPAC2 correlated with reduced relapse-free survival in patients with PDAC. VPAC2 activation in PDAC cells upregulated Piwi-like RNA-mediated gene silencing 2, which stimulated cancer cell clonogenic growth. In addition, VPAC2 signaling increased expression of TGFβ1 to inhibit T-cell function. Loss ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Sep","modification":"2026-06-01T07:18:22.77Z","creation":"2025-04-06T22:46:11.093Z"},"accession":"S-EPMC11458156","cross_references":{"pubmed":["38809694"],"doi":["10.1158/0008-5472.can-23-3628","10.1158/0008-5472.CAN-23-3628"]}}