{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T17:28:19Z","timestamp":1785432499958,"version":"3.56.0"},"posted":{"date-parts":[[2026,5,8]]},"group-title":"Cancer Biology","reference-count":58,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T00:00:00Z","timestamp":1778198400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"award":["PRE2018-083607"],"award-info":[{"award-number":["PRE2018-083607"]}],"id":[{"id":"https:\/\/ror.org\/05r0vyz12","id-type":"ROR","asserted-by":"publisher"}]},{"award":["PID2021-123372OB-I00"],"award-info":[{"award-number":["PID2021-123372OB-I00"]}],"id":[{"id":"https:\/\/ror.org\/05r0vyz12","id-type":"ROR","asserted-by":"publisher"}]},{"award":["CNS2023-143848"],"award-info":[{"award-number":["CNS2023-143848"]}],"id":[{"id":"https:\/\/ror.org\/05r0vyz12","id-type":"ROR","asserted-by":"publisher"}]},{"award":["PID2024-155980OB-I00"],"award-info":[{"award-number":["PID2024-155980OB-I00"]}],"id":[{"id":"https:\/\/ror.org\/05r0vyz12","id-type":"ROR","asserted-by":"publisher"}]},{"award":["PRE2022-101304"],"award-info":[{"award-number":["PRE2022-101304"]}],"id":[{"id":"https:\/\/ror.org\/05r0vyz12","id-type":"ROR","asserted-by":"publisher"}]},{"award":["LABAE211656TORR"],"award-info":[{"award-number":["LABAE211656TORR"]}],"id":[{"id":"https:\/\/ror.org\/00gxct719","id-type":"ROR","asserted-by":"publisher"}]},{"award":["EPAEC246710BIO"],"award-info":[{"award-number":["EPAEC246710BIO"]}],"id":[{"id":"https:\/\/ror.org\/00gxct719","id-type":"ROR","asserted-by":"publisher"}]},{"name":"Fundaci\u00f3n CRIS Contra el C\u00e1ncer","award":["PR_EX_2021-22"],"award-info":[{"award-number":["PR_EX_2021-22"]}]},{"name":"Fundaci\u00f3n CRIS Contra el C\u00e1ncer","award":["PR_TPD_2022-04"],"award-info":[{"award-number":["PR_TPD_2022-04"]}]},{"name":"National Institute for Health Care Management","award":["R01CA244780"],"award-info":[{"award-number":["R01CA244780"]}]},{"name":"National Institute for Health Care Management","award":["R61CA278402"],"award-info":[{"award-number":["R61CA278402"]}]},{"name":"National Institute for Health Care Management","award":["P30-CA196521"],"award-info":[{"award-number":["P30-CA196521"]}]},{"award":["Consolidator Grant 819242"],"award-info":[{"award-number":["Consolidator Grant 819242"]}],"id":[{"id":"https:\/\/ror.org\/0472cxd90","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,5,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>Despite the high curation rate of localized prostate cancer, the fraction of patients that progress to metastasis still accounts for thousands of deaths worldwide, underscoring the need to identify early molecular events that prime tumours for aggressive disease. Here, we demonstrate that loss of the metabolic transcriptional coactivator PGC1\u03b1 drives early extracellular matrix (ECM) remodelling in PCa, functionally linking epithelial transcriptional programs to tumour\u2013microenvironment interactions.<\/jats:p>\n                <jats:p>\n                  Using genetically engineered mouse models, we show that combined deletion of\n                  <jats:italic>Pten<\/jats:italic>\n                  and\n                  <jats:italic>Pgc1\u03b1<\/jats:italic>\n                  induces early activation of ECM-related transcriptional programs, increased collagen deposition, and a transition towards an aligned collagen fibre architecture\u2014hallmarks of aggressive disease\u2014prior to metastatic dissemination. Consistently, human prostate tumours with low PGC1\u03b1 expression display increased collagen deposition, supporting the clinical relevance of these findings. Restoration of PGC1\u03b1 expression in prostate cancer cells suppresses cell adhesion to multiple ECM substrates, disrupts collagen organization, and impairs tumour growth in a transcription-dependent manner.\n                <\/jats:p>\n                <jats:p>Through integrative matrisome proteomics and transcriptomics, we identify the secreted glycoprotein CTHRC1 as a key downstream effector that enhances the prognostic value of PGC1\u03b1 in PCa patients. Functional loss- and gain-of-function studies establish CTHRC1 expression as both necessary and sufficient to restore ECM adhesion, cytoskeletal organization, collagen architecture, and tumorigenic capacity in PGC1\u03b1-expressing cells. Importantly, recombinant CTHRC1 rescues adhesion defects, indicating that its extracellular pool mediates this phenotype, whereas deglycosylation abolishes its pro-adhesive function, revealing a mechanistic requirement for glycosylation.<\/jats:p>\n                <jats:p>Collectively, our findings uncover an early, cell-intrinsic ECM remodelling program driven by PGC1\u03b1 loss and identify the PGC1\u03b1\u2013CTHRC1 axis as a mechanistic and clinically relevant regulator of PCa aggressiveness.<\/jats:p>","DOI":"10.64898\/2026.05.05.722659","type":"posted-content","created":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T13:00:40Z","timestamp":1778245240000},"source":"Crossref","is-referenced-by-count":0,"title":["Loss of PGC1\u03b1 drives extracellular matrix remodelling in prostate cancer through CTHRC1"],"prefix":"10.64898","author":[{"given":"A","family":"Gonzalo-Paulano","sequence":"first","affiliation":[{"name":"Biochemistry and Molecular Biology Department, University of 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Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B","family":"Lectez","sequence":"additional","affiliation":[{"name":"Biochemistry and Molecular Biology Department, University of the Basque Country (UPV\/EHU), Leioa, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J","family":"Gardoki","sequence":"additional","affiliation":[{"name":"Biochemistry and Molecular Biology Department, University of the Basque Country (UPV\/EHU), Leioa, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I","family":"Lejona","sequence":"additional","affiliation":[{"name":"Biochemistry and Molecular Biology Department, University of the Basque Country (UPV\/EHU), Leioa, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"U","family":"Armendariz-Mart\u00ednez","sequence":"additional","affiliation":[{"name":"Biochemistry and Molecular Biology Department, University of the Basque Country (UPV\/EHU), Leioa, 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