ArticleMolecular biomedicine2025
LncRNA small nucleolar RNA host gene 1 (SNHG1) mediates acidic bile salt-induced EMT via the ULK1-Notch1 axis in Barrett's esophagus.
Article in Molecular biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Targeting the Notch signaling pathway in digestive system cancers: from bench to bedside.Cancer cell international · 2026Review
- Causal immune-inflammation mapping of the GERD-Barrett-adenocarcinoma cascade identifies FGF19-HLA-DR⁺ T-cell axis driving esophagogastric junction metaplasia.Journal of translational medicine · 2026Article
- Regulatory roles of LncRNAs in colorectal cancer immune evasion: current concepts and future perspectives.Discover oncology · 2025Review
- ULK1 gene polymorphisms and severe tuberculosis in the Chinese Han population: a case-control study.Frontiers in medicine · 2025Article
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9 authors.
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Abstract
Barrett's esophagus (BE) is a precancerous condition closely linked to chronic gastroesophageal reflux disease, characterized by the abnormal transformation of esophageal squamous mucosa into specialized intestinal-type epithelium, significantly elevating the risk of esophageal adenocarcinoma (EAC). Recurrent acidic bile reflux promotes epithelial-mesenchymal transition (EMT), a critical event driving malignant progression. However, the underlying molecular mechanisms remain incompletely understood. Here, we identify the long non-coding RNA small nucleolar RNA host gene 1 (SNHG1) as a novel regulator of EMT in BE, mediating its effects through the UNC-52-like kinase 1 (ULK1)-Notch1 signaling axis and autophagy modulation. Using BAR-T and CP-C cell models, we demonstrate that SNHG1 expression is elevated following acidic bile salt exposure, enhancing EMT characteristics by promoting the phosphorylation of ULK1 and activating Notch1 signaling. Pharmacological interventions targeting autophagy (Rapamycin) and Notch signaling (DAPT) further confirmed that SNHG1's effects on EMT are mediated via modulation of the autophagy-Notch1 interplay. We further validated our results in vivo using the previously described IL1β-induced Lgr5-CreERT2; p16
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