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<p>Glioblastoma (GBM) is a highly aggressive and lethal brain tumor, and despite conventional treatments, patient prognosis remains poor. Understanding the molecular mechanisms driving GBM and identifying potential therapeutic targets is critical. MOV10, an RNA helicase, is overexpressed in multiple cancers and is considered an oncogene. Our analysis of datasets from TCGA, GEO, and CGGA showed that MOV10 expression is elevated in GBM and strongly negatively correlated with overall survival (OS). Cox regression confirmed MOV10 as an independent prognostic risk factor for GBM.Functional enrichment analysis revealed that MOV10 is involved in immune regulation and tumor progression pathways. We found that MOV10 expression is closely linked to immune infiltration, immune checkpoint expression, and responses to immunotherapy. Immunofluorescence and Transwell assays confirmed that MOV10 knockdown reduced M2 macrophage migration and invasion in GBM cells. Clinical analysis further validated MOV10 overexpression in GBM tissues.In vitro, MOV10 silencing suppressed GBM cell proliferation, inhibited EMT-like processes, and promoted apoptosis through autophagy modulation. Our findings suggest that MOV10 plays a crucial role in GBM progression and could be a promising molecular target for therapy.</p>

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MOV10, a novel immunotherapy and prognostic biomarker, contributes to glioma development by regulating autophagy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月18日

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  • Feiyu Wang,
  • Linlin Ruan,
  • Wenbin Yang,
  • Yueben Hu,
  • Yangzhong Guo,
  • Xuanxuan Xiong,
  • Dan Liu,
  • Qiaoli Lv,
  • Shuhui Chen

摘要

Glioblastoma (GBM) is a highly aggressive and lethal brain tumor, and despite conventional treatments, patient prognosis remains poor. Understanding the molecular mechanisms driving GBM and identifying potential therapeutic targets is critical. MOV10, an RNA helicase, is overexpressed in multiple cancers and is considered an oncogene. Our analysis of datasets from TCGA, GEO, and CGGA showed that MOV10 expression is elevated in GBM and strongly negatively correlated with overall survival (OS). Cox regression confirmed MOV10 as an independent prognostic risk factor for GBM.Functional enrichment analysis revealed that MOV10 is involved in immune regulation and tumor progression pathways. We found that MOV10 expression is closely linked to immune infiltration, immune checkpoint expression, and responses to immunotherapy. Immunofluorescence and Transwell assays confirmed that MOV10 knockdown reduced M2 macrophage migration and invasion in GBM cells. Clinical analysis further validated MOV10 overexpression in GBM tissues.In vitro, MOV10 silencing suppressed GBM cell proliferation, inhibited EMT-like processes, and promoted apoptosis through autophagy modulation. Our findings suggest that MOV10 plays a crucial role in GBM progression and could be a promising molecular target for therapy.