{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen JL"],"funding":["Szu-Yuan Research Foundation of Internal Medicine","Melissa Lee Cancer Foundation","Taipei City Hospital","Taipei Veterans General Hospital","National Science and Technology Council","Dr. Morris Chang","Teh-Tzer Study Group for Human Medical Research Foundation of Taiwan"],"pagination":["345"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12578764"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(1)"],"pubmed_abstract":["Diffuse large B-cell lymphoma (DLBCL) is characterized by molecular complexity and heterogeneity. The SET oncoprotein is overexpressed in B-cell chronic lymphocytic leukemia and non-Hodgkin lymphoma. Acting as an intrinsic inhibitor of the tumor suppressor protein phosphatase 2A (PP2A), targeting SET has shown anti-cancer activity. In this study, we investigated the molecular mechanism of SET antagonism in DLBCL. Overexpression of SET resulted in decreased phosphatase activities of PP2A and SHP-1, while activating Lyn. Conversely, SET inhibition, either through antagonists or siRNA, led to the activation of PP2A and SHP-1, resulting in the inactivation of Lyn. Analysis of public datasets revealed upregulation of Lyn in late-stage DLBCL samples, which was associated with a worse outcome. Ec"],"journal":["Clinical and experimental medicine"],"pubmed_title":["Targeting SET to counteract Lyn activation demonstrates anti-cancer potential in diffuse large B-cell lymphoma."],"pmcid":["PMC12578764"],"funding_grant_id":["TPCH-113-37","NSTC 114-2811-B-A49A-004","V114C-013","ABMRD002","NSTC 112-2314-B-A49-083-MY3","B1131020"],"pubmed_authors":["Chang YY","Wang WL","Liu CY","Huang CT","Chu PY","Dai MS","Chen JL"],"additional_accession":[]},"is_claimable":false,"name":"Targeting SET to counteract Lyn activation demonstrates anti-cancer potential in diffuse large B-cell lymphoma.","description":"Diffuse large B-cell lymphoma (DLBCL) is characterized by molecular complexity and heterogeneity. The SET oncoprotein is overexpressed in B-cell chronic lymphocytic leukemia and non-Hodgkin lymphoma. Acting as an intrinsic inhibitor of the tumor suppressor protein phosphatase 2A (PP2A), targeting SET has shown anti-cancer activity. In this study, we investigated the molecular mechanism of SET antagonism in DLBCL. Overexpression of SET resulted in decreased phosphatase activities of PP2A and SHP-1, while activating Lyn. Conversely, SET inhibition, either through antagonists or siRNA, led to the activation of PP2A and SHP-1, resulting in the inactivation of Lyn. Analysis of public datasets revealed upregulation of Lyn in late-stage DLBCL samples, which was associated with a worse outcome. Ec","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-06-06T14:49:21.567Z","creation":"2026-06-01T03:07:29.997Z"},"accession":"S-EPMC12578764","cross_references":{"pubmed":["41171490"],"doi":["10.1007/s10238-025-01874-x"]}}