ArticleNature communications2025
EZH2 loss promotes gastric squamous cell carcinoma.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The RNA-binding protein La/SSB is associated with HNSCC progression and TFAP2C/FSCN1-linked transcriptional regulation.Oncogene · 2026Article
- T‑box transcription factor 15 regulated by methyltransferase‑like 3‑mediated N6‑methyladenosine modification promotes immune escape and progression of gastric cancer by activating matrix metalloproteinase 14 transcription.International journal of oncology · 2026Article
- ARID1A loss drives gastric signet ring cell carcinoma by regulating mucin production and secretion.Nature communications · 2026Article
- Acquired resistance of cancer therapies: Mechanisms and perspectives.Chinese medical journal · 2026Review
- From Tumor Biology to Clinical Perspectives: Novel Biomarkers and Therapeutic Insights in Gastric Cancer.Oncology research · 2026Review
- Overcoming diagnostic pitfalls in primary gastric squamous cell carcinoma: the imperative of adequate sampling in an elderly female patient, case report.Frontiers in oncology · 2025Article
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41 authors.
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Abstract
Gastric Squamous Cell Carcinoma (GSCC) is a rare but aggressive subtype of gastric cancer with unique histopathology, whose etiology remains poorly understood. Here, we perform genomics analyses of twenty GSCC samples and find that epigenetic regulation genes are among the most frequently mutated genes, including Enhancer of zeste homolog 2 (EZH2). Ezh2 loss induces squamous feature both in gastric organoids in vitro and in vivo mouse model. Ezh2 deficiency, together with Trp53 and Pten loss, both of which are also frequently mutated in GSCC, give rise to full-blown GSCC in mice. Mechanistically, we find that Ezh2 could repress the expression of Transcription factor AP-2 gamma (Tfap2c), a transcription factor with the ability to initiate epidermal squamous differentiation, through H3K27 methylation. Disruption of Tfap2c reduces the squamous characteristics of the Ezh2 loss-driven GSCC and reverses its resistance to chemo treatment. Our findings elucidate key molecular mechanisms underlying GSCC pathogenesis and identify potential therapeutic targets for this aggressive malignancy.
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