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Background <p>Gastric intestinal metaplasia (GIM) is a precancerous lesion closely associated with gastric cancer (GC) risk. A systematic characterization of the molecular profiles across distinct cell types during GIM progression is crucial for devising new intervention strategies and enabling early prevention for GC.</p> Methods <p>This study integrates single-cell transcriptomics and proteomics data from gastric tissues of patients with mild chronic non-atrophic gastritis (CNAG) and moderate-to-severe GIM.</p> Results <p>We identified differentially expressed genes (DEGs) and proteins (DEPs) that show consistent changes at both transcriptional and protein levels across epithelial, stromal, and immune cells. Notably, most proteins were downregulated in GIM tissues, potentially linked to reduced expression of RNA splicing-related genes. Epithelial cells in GIM lesions exhibited intestinal-type subpopulations, including goblet and enterocytes, likely originating from gastric isthmus stem cells. Despite overall protein downregulation, the ubiquitin-like protein NEDD8 was markedly upregulated in metaplastic tissues, especially in <i>H. pylori</i>-positive tissues. Pathways involved in cytoskeleton maintenance, extracellular matrix stability, and cell adhesion were downregulated, while several macrophage-expressed DEGs/DEPs (e.g., BST2, CYBB, ITGB2) were elevated.</p> Conclusions <p>This work delineates dynamic transcriptional and translational alterations during the progression from mild gastritis to GIM. It implies that chronic inflammatory injury causes suppress protein synthesis, further driving metaplastic transformation early gastric precancerous lesions.</p>

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A single-cell multi-omics atlas defines the cellular and molecular landscape of gastric intestinal metaplasia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月20日

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  • Yuman Ye,
  • Xiaomin Gong,
  • Sujuan Liu,
  • Na Hu,
  • Huijie Zhang,
  • Xiao Fei,
  • Aofei Huang,
  • Wentao Fan,
  • Zhenping Chen,
  • Huan Wang,
  • Xingxing He,
  • Yi Hu,
  • Nonghua Lu,
  • Yin Zhu,
  • Huajing Ke,
  • Nianshuang Li

摘要

Background

Gastric intestinal metaplasia (GIM) is a precancerous lesion closely associated with gastric cancer (GC) risk. A systematic characterization of the molecular profiles across distinct cell types during GIM progression is crucial for devising new intervention strategies and enabling early prevention for GC.

Methods

This study integrates single-cell transcriptomics and proteomics data from gastric tissues of patients with mild chronic non-atrophic gastritis (CNAG) and moderate-to-severe GIM.

Results

We identified differentially expressed genes (DEGs) and proteins (DEPs) that show consistent changes at both transcriptional and protein levels across epithelial, stromal, and immune cells. Notably, most proteins were downregulated in GIM tissues, potentially linked to reduced expression of RNA splicing-related genes. Epithelial cells in GIM lesions exhibited intestinal-type subpopulations, including goblet and enterocytes, likely originating from gastric isthmus stem cells. Despite overall protein downregulation, the ubiquitin-like protein NEDD8 was markedly upregulated in metaplastic tissues, especially in H. pylori-positive tissues. Pathways involved in cytoskeleton maintenance, extracellular matrix stability, and cell adhesion were downregulated, while several macrophage-expressed DEGs/DEPs (e.g., BST2, CYBB, ITGB2) were elevated.

Conclusions

This work delineates dynamic transcriptional and translational alterations during the progression from mild gastritis to GIM. It implies that chronic inflammatory injury causes suppress protein synthesis, further driving metaplastic transformation early gastric precancerous lesions.