ArticleJournal of cellular and molecular medicine2026
The STAT3-CCND2 Axis Drives a Proliferative Metaplastic Precursor Population in Gastric Intestinal Metaplasia.
Article in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Gastric intestinal metaplasia (GIM) is a crucial precancerous lesion with ill-defined drivers, and identifying regulators of its early proliferation and reprogramming is key to interception. We integrated epigenomic-transcriptomic analysis of human GIM and normal tissues, validated targets via dual-luciferase assay, and mapped cellular heterogeneity by single-cell RNA sequencing of patient-derived gastric organoids. Functional validation using organoids included STAT3 knockdown assessed by qRT-PCR and immunofluorescence. STAT3 was identified as a top regulator of hypomethylated, upregulated genes in GIM and directly transactivated CCND2. Single-cell analysis revealed a dominant proliferative "Cycling GIM-precursor" population co-expressing STAT3/CCND2. STAT3 knockdown reduced CCND2 and intestinal markers (CDX2, MUC2) in GIM organoids. The STAT3-CCND2 axis is central to early GIM pathogenesis, offering targets for early detection and chemoprevention of gastric cancer.
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