{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["20(9)"],"submitter":["Nam AY"],"pubmed_abstract":["Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related deaths, remaining a significant challenge in terms of early detection, effective treatment, and improving patient survival rates. In this study, we investigated the anticancer mechanism of rubiarbonol B (Ru-B) and its derivative 3-O-acetylrubiarbonol B (ARu-B), a pentacyclic terpenoid in gefitinib (GEF)-sensitive and -resistant NSCLC HCC827 cells. Concentration- and time-dependent cytotoxicity was observed for both Ru-B and ARu-B. The in vitro kinase assay showed that ARu-B treatment inhibited epidermal growth factor receptor (EGFR), mesenchymal-epithelial transition (MET), and AKT1, and their phosphorylation in HCC827 cells. A molecular docking model suggested that ARu-B could interact with EGFR and MET in d"],"journal":["PloS one"],"pagination":["e0329706"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12416685"],"repository":["biostudies-literature"],"pubmed_title":["3-O-acetylrubiarbonol B preferentially targets EGFR and MET over rubiarbonol B to inhibit NSCLC cell growth."],"pmcid":["PMC12416685"],"pubmed_authors":["Lee NY","Yoon G","Park JW","Shim JH","Na M","Nam AY","Joo SH"],"additional_accession":[]},"is_claimable":false,"name":"3-O-acetylrubiarbonol B preferentially targets EGFR and MET over rubiarbonol B to inhibit NSCLC cell growth.","description":"Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related deaths, remaining a significant challenge in terms of early detection, effective treatment, and improving patient survival rates. In this study, we investigated the anticancer mechanism of rubiarbonol B (Ru-B) and its derivative 3-O-acetylrubiarbonol B (ARu-B), a pentacyclic terpenoid in gefitinib (GEF)-sensitive and -resistant NSCLC HCC827 cells. Concentration- and time-dependent cytotoxicity was observed for both Ru-B and ARu-B. The in vitro kinase assay showed that ARu-B treatment inhibited epidermal growth factor receptor (EGFR), mesenchymal-epithelial transition (MET), and AKT1, and their phosphorylation in HCC827 cells. A molecular docking model suggested that ARu-B could interact with EGFR and MET in d","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-06-03T05:58:30.102Z","creation":"2026-04-25T03:16:54.736Z"},"accession":"S-EPMC12416685","cross_references":{"pubmed":["40920675"],"doi":["10.1371/journal.pone.0329706"]}}