{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T10:48:27Z","timestamp":1785408507912,"version":"3.56.0"},"posted":{"date-parts":[[2026,4,20]]},"group-title":"Cancer Biology","reference-count":69,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,4,20]],"date-time":"2026-04-20T00:00:00Z","timestamp":1776643200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"award":["P30CA044579"],"award-info":[{"award-number":["P30CA044579"]}],"id":[{"id":"https:\/\/ror.org\/040gcmg81","id-type":"ROR","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000048","name":"American Cancer Society","doi-asserted-by":"crossref","award":["PF-25-1513328-01-PFCBI Grant DO1#: https:\/\/doi.org\/10.53354\/ACS.PF-25-1513328-01-PFCBI.pc.gr.238167"],"award-info":[{"award-number":["PF-25-1513328-01-PFCBI Grant DO1#: https:\/\/doi.org\/10.53354\/ACS.PF-25-1513328-01-PFCBI.pc.gr.238167"]}],"id":[{"id":"10.13039\/100000048","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["U01 CA224012"],"award-info":[{"award-number":["U01 CA224012"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["P30 CA069533"],"award-info":[{"award-number":["P30 CA069533"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["U01 CA243007"],"award-info":[{"award-number":["U01 CA243007"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Ellen and Lake Cowart"},{"name":"The Oshrine Family"},{"DOI":"10.13039\/100019054","name":"The Farrell Family Foundation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100019054","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Hildegard Lam from Endowed Chair in Basic Research"},{"name":"OHSU Brenden-Colsson Center for Pancreatic Care"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,4,20]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Pancreatic adenocarcinoma (PDAC) is an abysmal disease, with a poor clinical outcome, largely due to limited life-extending treatments for patients. Notoriously, PDAC displays a T cell-suppressive tumor microenvironment where underlying molecular mechanisms that lead to this phenotype remain poorly understood. To unravel specific mechanisms, we utilized bioinformatic analyses with functional studies and revealed the cytolinker protein plectin (PLEC) as a novel player in regulating the T cell-suppressive tumor microenvironment of PDAC.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>\n                    Utilizing the TCGA-PAAD dataset, tumor samples were separated by PLEC expression to evaluate patient survival, and pathway analyses associated with increased tumorigenesis. Evaluation of immune infiltration and subsequent immune deconvolution was performed using tidyestimate and CIBERSORTx R packages. Single-cell RNA-seq (scRNA-seq) analysis from 229 PDAC patients was analyzed to investigate signaling dynamics and immune cell infiltration in PLEC\n                    <jats:sup>High<\/jats:sup>\n                    patients. Functional validation was provided using a monoclonal antibody (mAb) against cell surface plectin (CSP) in two murine PDAC models to examine changes in tumor growth and immune cell subset abundance.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\n                    Our studies revealed that high plectin expression results in an overall worse survival associated with activation of pro-tumorigenic pathways and decreased anti-tumor immune signature in PDAC patients. Analysis via GSEA indicates PLEC\n                    <jats:sup>High<\/jats:sup>\n                    patients display an aggressive phenotype and suppressed pro-inflammatory signaling pathways. Immune ESTIMATE scores were significantly decreased in PLEC\n                    <jats:sup>High<\/jats:sup>\n                    patients, and scRNA-seq analysis revealed that PLEC\n                    <jats:sup>High<\/jats:sup>\n                    tumors display a decrease in anti-tumor CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells.\n                    <jats:italic>In vivo<\/jats:italic>\n                    analyses using an anti-CSP mAb revealed a reduction in tumor growth kinetics compared to IgG control corresponding with a significant increase in proliferating and activated cytotoxic CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells. Anti-CSP-mediated tumor suppression was inhibited when CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells were depleted, indicating that anti-CSP treatment is contingent on cytotoxic T cell functionality.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>\n                    Our findings identify plectin as a biomarker of aggressive disease in PDAC, with high plectin expression associated with decreased T cell infiltration, and that treatment with anti-CSP mAb reinstates anti-tumor immunity and decreases tumor volume\n                    <jats:italic>in vivo<\/jats:italic>\n                    . These findings position plectin as a high-priority therapeutic target, with the potential to fundamentally reshape immune responses in PDAC and improve outcomes for patients with few remaining options.\n                  <\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.04.16.718901","type":"posted-content","created":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T04:00:18Z","timestamp":1776744018000},"source":"Crossref","is-referenced-by-count":0,"title":["Plectin promotes an aggressive phenotype and represses cytotoxic T cell activity in pancreatic cancer"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4769-9571","authenticated-orcid":false,"given":"Cody L.","family":"Wolf","sequence":"first","affiliation":[{"name":"Department of Biomedical Engineering, University of Virginia, Charlottesville, VA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roxanne 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USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5184-927X","authenticated-orcid":false,"given":"Karl M.","family":"Kowalewski","sequence":"additional","affiliation":[{"name":"Department of Chemical Engineering, University of Virginia, Charlottesville, VA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew J.","family":"Lazzara","sequence":"additional","affiliation":[{"name":"Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, VA, USA"},{"name":"Department of Chemical Engineering, University of Virginia, Charlottesville, VA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amanda","family":"Poissonnier","sequence":"additional","affiliation":[{"name":"Department of Cell, Developmental, & Cancer Biology, Oregon Health and Science University, Portland, OR, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa 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