ArticleCancer medicine2025
Identification of the Oncogenic Role of MSH2 in the Stemness and Progression of Glioma Through Regulating Wnt Signaling Pathway.
Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Systems biology of Wnt signaling in glioma chemotherapy resistance: Integrating multi-omics mechanisms and emerging therapeutic vulnerabilities (Review).Oncology letters · 2026Review
- Identification of the Oncogenic Role of MSH2 in the Stemness and Progression of Glioma Through Regulating Wnt Signaling Pathway.Cancer medicine · 2025Article
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Authors and funding
3 authors.
Funding
Abstract
backgroundGlioma is one of the most aggressive brain tumors, and its progression is often associated with stemness maintenance and therapy resistance. The role of MSH2 in glioma remains largely unclear.
methodsWe analyzed public datasets and clinical samples to assess MSH2 expression and its clinical relevance. Functional assays in vitro and in vivo were performed to investigate the effects of MSH2 knockdown on glioma cell behavior. Mechanistic studies were conducted to explore downstream signaling pathways and stemness regulation.
resultsMSH2 was found to be significantly upregulated in glioma tissues and cell lines, and its high expression correlated with poor prognosis. Silencing MSH2 inhibited cell proliferation, migration, and tumor growth, while promoting apoptosis and G2 cell cycle arrest. Mechanistically, phospho-kinase screening and rescue experiments suggested that MSH2 promotes glioma progression via activation of the Wnt/β-catenin signaling pathway. Furthermore, MSH2 knockdown suppressed the expression of stemness markers, impaired sphere formation, and sensitized glioma cells to cisplatin treatment.
conclusionsOur study identifies MSH2 as an oncogenic factor in glioma, which drives stemness and progression through regulation of the Wnt/β-catenin pathway, and may serve as a potential therapeutic target.
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