{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sanchez-Tillo E"],"funding":["Agència de Gestió d’Ajuts Universitaris i de Recerca","Spanish Ministry of Science and Innovation","Olga Torres Foundation","Spanish Association Against Cancer","Spanish National Institute of Health Carlos III"],"pagination":["e164629"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10619495"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(20)"],"pubmed_abstract":["Despite being in the same pathway, mutations of KRAS and BRAF in colorectal carcinomas (CRCs) determine distinct progression courses. ZEB1 induces an epithelial-to-mesenchymal transition (EMT) and is associated with worse progression in most carcinomas. Using samples from patients with CRC, mouse models of KrasG12D and BrafV600E CRC, and a Zeb1-deficient mouse, we show that ZEB1 had opposite functions in KRAS- and BRAF-mutant CRCs. In KrasG12D CRCs, ZEB1 was correlated with a worse prognosis and a higher number of larger and undifferentiated (mesenchymal or EMT-like) tumors. Surprisingly, in BrafV600E CRC, ZEB1 was associated with better prognosis; fewer, smaller, and more differentiated (reduced EMT) primary tumors; and fewer metastases. ZEB1 was positively correlated in KRAS-mutant CRC c"],"journal":["JCI insight"],"pubmed_title":["The EMT factor ZEB1 paradoxically inhibits EMT in BRAF-mutant carcinomas."],"pmcid":["PMC10619495"],"funding_grant_id":["2017-SGR-1174","2021-SGR-01328","AECC,PROYE19040POST_001","PID2020-116338RB-I00","CP13/00200,PI18/00244","SAF2017-84918-R","Biannual Grant A-2019/2020"],"pubmed_authors":["Siles L","Pedrosa L","Darling DS","Lozano JJ","Sanchez-Moral L","Vila I","Esteve-Codina A","Postigo A","Castells A","Sanchez-Tillo E","Maurel J","Gyorffy B","Cuatrecasas M","Chen Y"],"additional_accession":[]},"is_claimable":false,"name":"The EMT factor ZEB1 paradoxically inhibits EMT in BRAF-mutant carcinomas.","description":"Despite being in the same pathway, mutations of KRAS and BRAF in colorectal carcinomas (CRCs) determine distinct progression courses. ZEB1 induces an epithelial-to-mesenchymal transition (EMT) and is associated with worse progression in most carcinomas. Using samples from patients with CRC, mouse models of KrasG12D and BrafV600E CRC, and a Zeb1-deficient mouse, we show that ZEB1 had opposite functions in KRAS- and BRAF-mutant CRCs. In KrasG12D CRCs, ZEB1 was correlated with a worse prognosis and a higher number of larger and undifferentiated (mesenchymal or EMT-like) tumors. Surprisingly, in BrafV600E CRC, ZEB1 was associated with better prognosis; fewer, smaller, and more differentiated (reduced EMT) primary tumors; and fewer metastases. ZEB1 was positively correlated in KRAS-mutant CRC c","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Oct","modification":"2026-05-29T12:18:55.737Z","creation":"2025-04-20T01:34:12.337Z"},"accession":"S-EPMC10619495","cross_references":{"pubmed":["37870961"],"doi":["10.1172/jci.insight.164629"]}}