{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li C"],"funding":["China Scholarship Council","ZonMw","ZonMw grant"],"pagination":["3103-3112"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12599596"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["599(21)"],"pubmed_abstract":["ERBIN acts as a negative regulator of the epidermal growth factor receptor (EGFR) and transforming growth factor-β (TGF-β)/SMAD signaling pathways that play a role in epithelial-to-mesenchymal transition (EMT). However, the role of ERBIN in EMT is poorly understood. Our results show that ERBIN inhibits TGF-β-induced EMT in NMuMG breast and in A549 lung adenocarcinoma cell lines. ERBIN inhibits TGF-β/SMAD-dependent gene expression and also interferes with TGF-β-induced extracellular signal-regulated kinase (ERK) phosphorylation. Moreover, when the TGF-β type I receptor kinase activity is inhibited, the mesenchymal state of ERBIN-depleted A549 cells is reduced. Pharmacological inhibition of TGF-β receptor and EGFR signaling counteracts increased EMT and migration in A549 ERBIN-depleted cells. Our findings identify ERBIN as a key suppressor of EMT through coordinated inhibition of TGF-β and EGFR signaling pathways."],"journal":["FEBS letters"],"pubmed_title":["ERBIN limits epithelial cell plasticity via suppression of TGF-β signaling."],"pmcid":["PMC12599596"],"funding_grant_id":["09120012010061"],"pubmed_authors":["Ten Dijke P","Li C","van der Zon G","Shen T"],"additional_accession":[]},"is_claimable":false,"name":"ERBIN limits epithelial cell plasticity via suppression of TGF-β signaling.","description":"ERBIN acts as a negative regulator of the epidermal growth factor receptor (EGFR) and transforming growth factor-β (TGF-β)/SMAD signaling pathways that play a role in epithelial-to-mesenchymal transition (EMT). However, the role of ERBIN in EMT is poorly understood. Our results show that ERBIN inhibits TGF-β-induced EMT in NMuMG breast and in A549 lung adenocarcinoma cell lines. ERBIN inhibits TGF-β/SMAD-dependent gene expression and also interferes with TGF-β-induced extracellular signal-regulated kinase (ERK) phosphorylation. Moreover, when the TGF-β type I receptor kinase activity is inhibited, the mesenchymal state of ERBIN-depleted A549 cells is reduced. Pharmacological inhibition of TGF-β receptor and EGFR signaling counteracts increased EMT and migration in A549 ERBIN-depleted cells. Our findings identify ERBIN as a key suppressor of EMT through coordinated inhibition of TGF-β and EGFR signaling pathways.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-05T12:24:13.086Z","creation":"2026-05-16T03:12:57.155Z"},"accession":"S-EPMC12599596","cross_references":{"pubmed":["40859866"],"doi":["10.1002/1873-3468.70121"]}}