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https://www.selleckchem.com/products/mrtx849.html Functionally, LINC01980 acted as a competitively endogenous RNA (ceRNA) to impact the expression of MYO5A by sponging miR-190a-5p in ESCC. Therefore, these findings suggest that LINC01980 may act as an oncogenic lncRNA in ESCC and LINC01980/miR-190a-5p/MYO5A pathway contributes to the development of ESCC. BACKGROUND & AIMS Studies are needed to determine the mechanism by which Barrett´s esophagus (BE) progresses to esophageal adenocarcinoma (EAC). Notch signaling maintains stem cells in the gastrointestinal tract and is dysregulated during carcinogenesis. We explored the relationship between Notch signaling and goblet cell maturation, a feature of BE, during EAC pathogenesis. METHODS We measured goblet cell density and levels of Notch mRNAs in BE tissues from 164 patients, with and without dysplasia or EAC, enrolled in a multicenter study. We analyzed the effects of conditional expression of an activated form of NOTCH2 (pL2.Lgr5.N2IC), conditional deletion of NOTCH2 (pL2.Lgr5.N2fl/fl), or loss of NF-κB (pL2.Lgr5.p65fl/fl), in Lgr5+ (progenitor) cells in L2-IL1B mice (overexpresses interleukin 1 beta in esophagus and squamous forestomach and are used as a model of BE). We collected esophageal and stomach tissues and performed histology, immunohistochemistry, flow cytometry, transcriptome, and real-time PCR anal metaplasia scores than pL2.Lgr5.N2IC mice. In organoids derived from pL2-IL1B mice, the NF-κB inhibitor JSH-23 reduced cell survival and proliferation. CONCLUSIONS Notch signaling contributes to activation of NF-κB and regulates differentiation of gastric cardia progenitor cells in a mouse model of BE. In human esophageal tissues, progression of BE to EAC associated with reduced goblet cell density and increased levels of Notch expression. Strategies to block this pathway might be developed to prevent EAC in patients with BE. Regulation of transcription and replication by the tetrad patterns of DNA has drawn th

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