{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lee J"],"funding":["NIDDK NIH HHS","NIAID NIH HHS","NINDS NIH HHS"],"pagination":["18182-9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3365759"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["287(22)"],"pubmed_abstract":["STAT3 was recently reported to suppress tumor invasion in Apc(min)(/+) mice. We investigated the mechanisms by which STAT3 inhibits intestinal epithelial tumors using Apc(min)(/+)/Stat3(IEC-KO) mice (intestinal epithelial cell (IEC)-specific deletion of STAT3 in the Apc(min)(/+) background) to determine the role of STAT3 in carcinogenesis in vivo as well as colorectal cancer cell lines in vitro. To inhibit invasion of IEC tumors, STAT3 functions as a molecular adaptor rather than a transcription factor. Accordingly, the tumors in Apc(min)(/+)/Stat3(IEC-KO) mice undergo adenoma-to-carcinoma transition and acquire an invasive phenotype. Similarly, STAT3 knockdown in a colorectal cell line enhances IEC invasion. We demonstrate that STAT3 down-regulates SNAI (Snail-1) expression levels and hence suppresses epithelial-mesenchymal transition of colorectal cancer cells. Mechanistically, STAT3 facilitates glycogen synthase kinase (GSK) 3β-mediated degradation of SNAI by regulating phosphorylation of GSK3β. Our data identified a new role for STAT3 in the adenoma-to-carcinoma sequence of intestinal tumors."],"journal":["The Journal of biological chemistry"],"pubmed_title":["Signal transducer and activator of transcription 3 (STAT3) protein suppresses adenoma-to-carcinoma transition in Apcmin/+ mice via regulation of Snail-1 (SNAI) protein stability."],"pmcid":["PMC3365759"],"funding_grant_id":["P30 NS047101","R01 AI068685","R24 DK080506","AI068685","P01 DK035108","DK35108","AI095623","DK080506","U01 AI095623"],"pubmed_authors":["Herdman S","Raz E","Kim H","Lee J","Lee SE","Kim JC","Quinley C","Corr M"],"additional_accession":[]},"is_claimable":false,"name":"Signal transducer and activator of transcription 3 (STAT3) protein suppresses adenoma-to-carcinoma transition in Apcmin/+ mice via regulation of Snail-1 (SNAI) protein stability.","description":"STAT3 was recently reported to suppress tumor invasion in Apc(min)(/+) mice. We investigated the mechanisms by which STAT3 inhibits intestinal epithelial tumors using Apc(min)(/+)/Stat3(IEC-KO) mice (intestinal epithelial cell (IEC)-specific deletion of STAT3 in the Apc(min)(/+) background) to determine the role of STAT3 in carcinogenesis in vivo as well as colorectal cancer cell lines in vitro. To inhibit invasion of IEC tumors, STAT3 functions as a molecular adaptor rather than a transcription factor. Accordingly, the tumors in Apc(min)(/+)/Stat3(IEC-KO) mice undergo adenoma-to-carcinoma transition and acquire an invasive phenotype. Similarly, STAT3 knockdown in a colorectal cell line enhances IEC invasion. We demonstrate that STAT3 down-regulates SNAI (Snail-1) expression levels and hence suppresses epithelial-mesenchymal transition of colorectal cancer cells. Mechanistically, STAT3 facilitates glycogen synthase kinase (GSK) 3β-mediated degradation of SNAI by regulating phosphorylation of GSK3β. Our data identified a new role for STAT3 in the adenoma-to-carcinoma sequence of intestinal tumors.","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 May","modification":"2024-10-16T03:26:44.575Z","creation":"2019-03-27T00:54:04Z"},"accession":"S-EPMC3365759","cross_references":{"pubmed":["22496368"],"doi":["10.1074/jbc.m111.328831","10.1074/jbc.M111.328831"]}}