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Transcription factor-mediated intestinal metaplasia and the role of a shadow enhancer

ABSTRACT: Epigenetic analysis on mouse gastric organoids overexpressing either CDX2, HNF4A or control GFP. Epigenetic analyses include ATAC-seq, Cut&Run. Mouse gastric and intestinal stem cell ATAC-seq and mouse gastric antrum and intestinal villus ChIP-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE160264 | GEO | 2022/02/21

REPOSITORIES: GEO

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Distinct processes and transcriptional targets underlie CDX2 requirements in intestinal stem cells and differentiated villus cells

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Metabolomics Workbench ST000354 - GNPS - Metabolite comparison of mouse gastric tissue and glands

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OLFM4 promotes the progression of intestinal metaplasia through MYH9/GSK3β/β-catenin pathway

Project description:Intestinal metaplasia (IM), precancerous lesions of gastric carcinoma (PLGC) induced by factors like nitrite, Helicobacter pylori, or bile acid, carries a high risk of progressing to gastric cancer. IM is categorized into complete intestinal metaplasia (CIM) and incomplete intestinal metaplasia (IIM). Patients with IIM are at a higher risk of developing gastric cancer, emphasizing its importance for early screening. Besides the diagnostic challenges, the mechanisms underlying its progression remain a mystery. OLFM4, a gene associated with stemness characteristics, has been linked to promoting gastric and colorectal cancers. Our investigation used pathological sections from two clinical centers, biopsies of IM tissues, PLGC cell models, animal models, and organoids to explore OLFM4's role in IIM. OLFM4 expression was observed highly in IIM, with superior diagnostic accuracy of IIM compared to CDX2 and MUC2 for the first time. OLFM4, along with MYH9, was highly expressed in IM organoids and PLGC animal models. OLFM4, in combination with MYH9, accelerated the ubiquitination of GSK3β and resulted in increased β-catenin levels through the Wnt signaling pathway, finally promoting the proliferation and invasion abilities of PLGC cells. In conclusion, OLFM4 serves as a novel biomarker for IIM and is utilized as an important auxiliary means to delimit the key population for early gastric cancer screening. This study provides new insights into the mechanisms of progression and a new target of therapy in intestinal metaplasia.

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