{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T23:19:32Z","timestamp":1782861572272,"version":"3.54.5"},"reference-count":43,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T00:00:00Z","timestamp":1773014400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T00:00:00Z","timestamp":1773014400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100004431","name":"Fondation de France","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004431","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004097","name":"Fondation ARC pour la Recherche sur le Cancer","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004097","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Science"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Patients with triple\u2010negative breast cancer (ER\n                    <jats:sup>\u2212<\/jats:sup>\n                    , PR\n                    <jats:sup>\u2212<\/jats:sup>\n                    , and HER2\n                    <jats:sup>\u2212<\/jats:sup>\n                    ) are routinely treated with chemotherapies that induce DNA damage. However, around 30% of patients display resistance, owing largely to increased DNA repair mechanisms, upregulated to allow cancer cells to escape such therapies. PRMT1 and PRMT5, the two main protein arginine methyltransferases, are involved in several biological pathways, including DNA repair signaling, where they contribute to ensuring DNA integrity. We then speculated that targeting their enzymatic activity may sensitize TNBC cells to chemotherapeutic agents inducing DNA double\u2010strand breaks. Here, we showed that PRMT1 and PRMT5 are recruited to DNA double\u2010strand breaks upon doxorubicin or carboplatin treatment, two chemotherapies currently used to treat TNBC patients, and are preferentially involved in the homologous recombination pathway. By combining PRMT inhibitors with doxorubicin or carboplatin, we increased DNA double\u2010strand breaks and impaired TNBC cell proliferation and clonogenicity in\u00a0vitro and sensitized patient\u2010derived models of TNBC to carboplatin treatment. These preclinical data provide a rationale for the clinical evaluation of PRMT inhibitors as combinatorial agents to improve chemotherapy efficacy for TNBC patients.\n                  <\/jats:p>","DOI":"10.1111\/cas.70338","type":"journal-article","created":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T16:40:07Z","timestamp":1773074407000},"page":"1273-1285","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Targeting PRMTs Creates Vulnerability of DNA Double\u2010Stand Break Repair Pathways, and Potentiates Chemotherapy Efficacy in TNBC"],"prefix":"10.1111","volume":"117","author":[{"given":"Charl\u00e8ne","family":"Thiebaut","sequence":"first","affiliation":[{"name":"Universit\u00e9 Claude Bernard Lyon 1  Lyon France"},{"name":"Inserm U1052 Centre de Recherche en Canc\u00e9rologie de Lyon  Lyon France"},{"name":"CNRS UMR5286 Centre de Recherche en Canc\u00e9rologie de Lyon  Lyon France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S\u00e9bastien","family":"Martinez","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Claude Bernard Lyon 1  Lyon France"},{"name":"Inserm U1052 Centre de Recherche en Canc\u00e9rologie de Lyon  Lyon France"},{"name":"CNRS UMR5286 Centre de Recherche en Canc\u00e9rologie de Lyon  Lyon France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ludivine","family":"Pruvost","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Claude Bernard Lyon 1  Lyon France"},{"name":"Inserm U1052 Centre de Recherche en Canc\u00e9rologie de Lyon  Lyon France"},{"name":"CNRS UMR5286 Centre de Recherche en Canc\u00e9rologie de Lyon  Lyon France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Louisane","family":"Eve","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Claude Bernard Lyon 1  Lyon France"},{"name":"Inserm U1052 Centre de Recherche en Canc\u00e9rologie de Lyon  Lyon France"},{"name":"CNRS UMR5286 Centre de Recherche en Canc\u00e9rologie de Lyon  Lyon France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rania","family":"El\u2010Botty","sequence":"additional","affiliation":[{"name":"Laboratory of Preclinical Investigation, Translational Research Department Institut Curie, PSL University  Paris France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Sourd","sequence":"additional","affiliation":[{"name":"Laboratory of Preclinical Investigation, Translational Research Department Institut Curie, PSL University  Paris France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elodie","family":"Montaudon","sequence":"additional","affiliation":[{"name":"Laboratory of Preclinical Investigation, Translational Research Department Institut Curie, PSL University  Paris 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