{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Odarenko KV"],"funding":["Russian state-funded project for ICBFM SB RAS","Russian Science Foundation"],"pagination":["11850"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12732811"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(24)"],"pubmed_abstract":["A disintegrin and metalloproteinase with thrombospondin motifs 6 (ADAMTS6) is an extracellular matrix (ECM) protease that promotes the invasion of lung adenocarcinoma (LUAD) cells. Herein, we investigate its role in epithelial-mesenchymal transition (EMT), a process that drives metastasis and drug resistance in LUAD. Re-analysis of microarray and RNA sequencing data from LUAD cells revealed that during EMT, TGF-β1 increased <i>ADAMTS6</i> expression, presumably through the SMAD pathway, as SMAD2 loss completely blocked this effect. Moreover, <i>ADAMTS6</i> was shown to occupy hub positions within TGF-β1-associated gene networks. Using additional datasets, we found that <i>ADAMTS6</i> expression increased under other EMT-inducing conditions, including IL-1β induction and acquired gefitinib "],"journal":["International journal of molecular sciences"],"pubmed_title":["Deciphering the Role of ADAMTS6 in the Epithelial-Mesenchymal Transition of Lung Adenocarcinoma Cells."],"pmcid":["PMC12732811"],"funding_grant_id":["19-74-30011","125012300659-6","125012300660-2"],"pubmed_authors":["Odarenko KV","Zenkova MA","Markov AV","Stepanov GA","Matveeva AM"],"additional_accession":[]},"is_claimable":false,"name":"Deciphering the Role of ADAMTS6 in the Epithelial-Mesenchymal Transition of Lung Adenocarcinoma Cells.","description":"A disintegrin and metalloproteinase with thrombospondin motifs 6 (ADAMTS6) is an extracellular matrix (ECM) protease that promotes the invasion of lung adenocarcinoma (LUAD) cells. Herein, we investigate its role in epithelial-mesenchymal transition (EMT), a process that drives metastasis and drug resistance in LUAD. Re-analysis of microarray and RNA sequencing data from LUAD cells revealed that during EMT, TGF-β1 increased <i>ADAMTS6</i> expression, presumably through the SMAD pathway, as SMAD2 loss completely blocked this effect. Moreover, <i>ADAMTS6</i> was shown to occupy hub positions within TGF-β1-associated gene networks. Using additional datasets, we found that <i>ADAMTS6</i> expression increased under other EMT-inducing conditions, including IL-1β induction and acquired gefitinib ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-05-27T03:14:06.539Z","creation":"2026-05-27T03:11:16.651Z"},"accession":"S-EPMC12732811","cross_references":{"pubmed":["41465277"],"doi":["10.3390/ijms262411850"]}}