{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen Z"],"funding":["National Institutes of Health National Cancer Institute","NCI NIH HHS","National Institutes of Health"],"pagination":["218010"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12458680"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["633"],"pubmed_abstract":["c-Myc inhibition is a critical mechanism in mediating the therapeutic efficacy of osimertinib against EGFR mutant (EGFRm) NSCLCs and accordingly targeting c-Myc is an effective strategy for overcoming osimertinib acquired resistance, a challenging issue in the clinic. However, lack of specific c-Myc inhibitors restricts the application of this strategy. The current study focused on determining the potential application of an alternative c-Myc inhibitory approach to overcome osimertinib acquired resistance via targeting the MKK3/c-Myc interaction that stabilizes c-Myc protein. SGI-1027, as the first disruptor of MKK3/c-Myc interaction, effectively decreased c-Myc levels via disrupting this interaction and promoting c-Myc degradation in different osimertinib-resistant EGFRm NSCLC cell lines "],"journal":["Cancer letters"],"pubmed_title":["Targeting MKK3/c-Myc interaction to overcome osimertinib acquired resistance in EGFR mutant lung cancer."],"pmcid":["PMC12458680"],"funding_grant_id":["UG1 CA233259","P01 CA257906","R01 CA284386","R01 CA245386","R01 CA223220","P50 CA217691"],"pubmed_authors":["Ramalingam SS","Chen Z","Fu H","Wang D","Vallega KA","Bildtsen E","Ivanov AA","Sun SY"],"additional_accession":[]},"is_claimable":false,"name":"Targeting MKK3/c-Myc interaction to overcome osimertinib acquired resistance in EGFR mutant lung cancer.","description":"c-Myc inhibition is a critical mechanism in mediating the therapeutic efficacy of osimertinib against EGFR mutant (EGFRm) NSCLCs and accordingly targeting c-Myc is an effective strategy for overcoming osimertinib acquired resistance, a challenging issue in the clinic. However, lack of specific c-Myc inhibitors restricts the application of this strategy. The current study focused on determining the potential application of an alternative c-Myc inhibitory approach to overcome osimertinib acquired resistance via targeting the MKK3/c-Myc interaction that stabilizes c-Myc protein. SGI-1027, as the first disruptor of MKK3/c-Myc interaction, effectively decreased c-Myc levels via disrupting this interaction and promoting c-Myc degradation in different osimertinib-resistant EGFRm NSCLC cell lines ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-05-30T03:11:11.998Z","creation":"2026-05-30T03:07:03.727Z"},"accession":"S-EPMC12458680","cross_references":{"pubmed":["40886822"],"doi":["10.1016/j.canlet.2025.218010"]}}