{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T07:54:01Z","timestamp":1790927641544,"version":"4.1.0"},"reference-count":62,"publisher":"American Association for Cancer Research (AACR)","issue":"10","funder":[{"DOI":"10.13039\/100000048","name":"American Cancer Society","doi-asserted-by":"publisher","award":["21\u2013143-01-IRG"],"award-info":[{"award-number":["21\u2013143-01-IRG"]}],"id":[{"id":"10.13039\/100000048","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","award":["CA013106"],"award-info":[{"award-number":["CA013106"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["CA249002"],"award-info":[{"award-number":["CA249002"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","award":["CA211506"],"award-info":[{"award-number":["CA211506"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100002645","name":"Carol M. Baldwin Breast Cancer Research Fund","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100002645","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100005979","name":"Lustgarten Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100005979","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["aacrjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,10,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy primarily driven by oncogenic KRAS signaling. The splicing factor serine\/arginine-rich splicing factor 1 (SRSF1) plays a key oncogenic role in PDAC through reciprocal cross-interactions with KRAS signaling. However, the mechanisms regulating SRSF1 protein stability remain poorly understood. In this study, we identify the deubiquitinase USP39 as a critical regulator of SRSF1 stability. It interacts with SRSF1 in an RNA-independent manner and suppresses its ubiquitination. USP39 is upregulated in PDAC and correlates with poor patient prognosis. Functional analyses demonstrate that USP39 promotes PDAC cell progression, in part through the stabilization of SRSF1. Mechanistically, MYC activates USP39 transcription through direct promoter binding. These findings define a MYC\u2013USP39\u2013SRSF1 regulatory axis that integrates transcriptional and posttranslational mechanisms in PDAC and suggest USP39 as a potential therapeutic target.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Implications:<\/jats:title>\n                    <jats:p>USP39 functions as a central regulator that integrates transcriptional and posttranslational regulation in pancreatic cancer through the MYC\u2013USP39\u2013SRSF1 axis and represents a potential therapeutic target.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1158\/1541-7786.mcr-25-1104","type":"journal-article","created":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T14:00:13Z","timestamp":1781186413000},"page":"837-848","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["MYC-Mediated USP39 Upregulation Stabilizes SRSF1 in Pancreatic Cancer"],"prefix":"10.1158","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-6851-2486","authenticated-orcid":false,"given":"Benteng","family":"Ma","sequence":"first","affiliation":[{"name":"1Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York."},{"name":"2Molecular and Cell Biology Graduate Program, State University of New York at Stony Brook, Stony Brook, New York."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-3880-8891","authenticated-orcid":false,"given":"Xin","family":"Zhang","sequence":"additional","affiliation":[{"name":"1Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-5462-0296","authenticated-orcid":false,"given":"Alexander 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Spring Harbor, New York."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4403-1277","authenticated-orcid":false,"given":"Paolo","family":"Cifani","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02qz8b764","id-type":"ROR","asserted-by":"publisher"}],"name":"Cold Spring Harbor Laboratory 3 , Cold Spring Harbor, New York."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1169-6739","authenticated-orcid":false,"given":"Youngkyu","family":"Park","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02qz8b764","id-type":"ROR","asserted-by":"publisher"}],"name":"Cold Spring Harbor Laboratory 3 , Cold Spring Harbor, New York."},{"name":"4Lustgarten Foundation Pancreatic Cancer Research Laboratory, Cold Spring Harbor, New 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