{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Feingold PL"],"funding":["National Cancer Institute CCR NIH","Intramural NIH HHS","NCI NIH HHS"],"pagination":["2013-2023"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7643317"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(9)"],"pubmed_abstract":["In 2017, an estimated 17,000 individuals were diagnosed with esophageal adenocarcinoma (EAC), and less than 20% will survive 5 years. Positron emission tomography avidity is indicative of high glucose utilization and is nearly universal in EAC. TXNIP blocks glucose uptake and exhibits proapoptotic functions. Higher expression in EAC has been associated with improved disease-specific survival, lack of lymph node involvement, reduced perineural invasion, and increased tumor differentiation. We hypothesized that TXNIP may act as a tumor suppressor that sensitizes EAC cells to standard chemotherapeutics. EAC cell lines and a Barrett epithelial cell line were used. qRT-PCR, immunoblot, and immunofluorescence techniques evaluated gene expression. TXNIP was stably overexpressed or knocked down us"],"journal":["Molecular cancer therapeutics"],"pubmed_title":["Induction of Thioredoxin-Interacting Protein by a Histone Deacetylase Inhibitor, Entinostat, Is Associated with DNA Damage and Apoptosis in Esophageal Adenocarcinoma."],"pmcid":["PMC7643317"],"funding_grant_id":["ZIA BC 011630","ZIA BC011630-04","ZIA BC011630"],"pubmed_authors":["Lee S","McLoughlin KC","Nancarrow DJ","Hoang CD","Trepel JB","Hernandez JM","Ripley RT","Beer DG","Surman DR","Xi S","Shukla V","Schrump DS","Crooks DR","McDuffie LA","Brown K","Diggs LP","Feingold PL","Davis JL","Reardon ES","Gao S","Neckers LM","Xu Y","Lee MJ"],"additional_accession":[]},"is_claimable":false,"name":"Induction of Thioredoxin-Interacting Protein by a Histone Deacetylase Inhibitor, Entinostat, Is Associated with DNA Damage and Apoptosis in Esophageal Adenocarcinoma.","description":"In 2017, an estimated 17,000 individuals were diagnosed with esophageal adenocarcinoma (EAC), and less than 20% will survive 5 years. Positron emission tomography avidity is indicative of high glucose utilization and is nearly universal in EAC. TXNIP blocks glucose uptake and exhibits proapoptotic functions. Higher expression in EAC has been associated with improved disease-specific survival, lack of lymph node involvement, reduced perineural invasion, and increased tumor differentiation. We hypothesized that TXNIP may act as a tumor suppressor that sensitizes EAC cells to standard chemotherapeutics. EAC cell lines and a Barrett epithelial cell line were used. qRT-PCR, immunoblot, and immunofluorescence techniques evaluated gene expression. TXNIP was stably overexpressed or knocked down us","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Sep","modification":"2025-04-19T23:20:23.729Z","creation":"2025-04-19T23:20:23.729Z"},"accession":"S-EPMC7643317","cross_references":{"pubmed":["29934340"],"doi":["10.1158/1535-7163.MCT-17-1240","10.1158/1535-7163.mct-17-1240"]}}