{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["46(1)"],"submitter":["Liu ZY"],"pubmed_abstract":["The transcription factor STAT3 is a promising target for the treatment of non-small cell lung cancer (NSCLC). STAT3 activity is mainly dependent on phosphorylation at tyrosine 705 (pSTAT3-Y705), but the modulation on pSTAT3-Y705 is elusive. By screening a library of deubiquitinases (Dubs), we found that the Otub1 increases STAT3 transcriptional activity. As a Dub, Otub1 binds to pSTAT3-Y705 and specifically abolishes its K48-linked ubiquitination, therefore preventing its degradation and promoting NSCLC cell survival. The Otub1/pSTAT3-Y705 axis could be a potential target for the treatment of NSCLC. To explore this concept, we screen libraries of FDA-approved drugs and natural products based on STAT3-recognition element-driven luciferase assay, from which crizotinib is found to block pSTAT"],"journal":["Acta pharmacologica Sinica"],"pagination":["184-195"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11697133"],"repository":["biostudies-literature"],"pubmed_title":["Inhibiting the Otub1/phosphorylated STAT3 axis for the treatment of non-small cell lung cancer."],"pmcid":["PMC11697133"],"pubmed_authors":["He YM","Ou YJ","Jiang QY","Li PF","Mao XL","Zhang YW","Ren Y","Zhuang HX","Liu ZY"],"additional_accession":[]},"is_claimable":false,"name":"Inhibiting the Otub1/phosphorylated STAT3 axis for the treatment of non-small cell lung cancer.","description":"The transcription factor STAT3 is a promising target for the treatment of non-small cell lung cancer (NSCLC). STAT3 activity is mainly dependent on phosphorylation at tyrosine 705 (pSTAT3-Y705), but the modulation on pSTAT3-Y705 is elusive. By screening a library of deubiquitinases (Dubs), we found that the Otub1 increases STAT3 transcriptional activity. As a Dub, Otub1 binds to pSTAT3-Y705 and specifically abolishes its K48-linked ubiquitination, therefore preventing its degradation and promoting NSCLC cell survival. The Otub1/pSTAT3-Y705 axis could be a potential target for the treatment of NSCLC. To explore this concept, we screen libraries of FDA-approved drugs and natural products based on STAT3-recognition element-driven luciferase assay, from which crizotinib is found to block pSTAT","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2026-06-06T19:56:36.893Z","creation":"2026-06-04T03:12:27.452Z"},"accession":"S-EPMC11697133","cross_references":{"pubmed":["39198663"],"doi":["10.1038/s41401-024-01366-w"]}}