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<p>G protein-coupled receptors (GPCRs) play a pivotal role in maintaining the stemness of both normal and cancer stem cells. However, the function of the regulator of G protein signaling (RGS) family, particularly in tumor stem cells, remains poorly under-stood. Through bioinformatics analysis of clinical data, we identified RGS20 as a potential regulator of glioma stemness and temozolomide (TMZ) resistance, which may significantly influence patient prognosis. Subsequent in vitro and in vivo experiments demonstrated that RGS20 inhibition markedly enhanced tumor sphere formation and upregulated stem cell markers by intrinsically activating the WNT/β-catenin signaling pathway, thereby promoting tumorigenesis and ultimately leading to TMZ resistance. Furthermore, in human glioblastoma specimens, β-catenin signaling associated with low RGS20 expression was significantly enriched in hypoxic regions, suggesting that this mechanism may support the maintenance of glioma stem cells (GSCs) and drive TMZ resistance within the hypoxic niche. Our findings reveal that low RGS20 expression sustains WNT/β-catenin signaling in a ligand-reduced manner within hypoxic niches, unveiling a novel intracellular mechanism that drives glioma progression. Targeting this mechanism could provide new therapeutic strategies for glioma treatment.</p>

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RGS20 reduces glioma stemness and temozolomide resistance by intrinsically inhibiting the WNT/β-catenin signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月28日

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  • Yang Xie,
  • Qi Li,
  • Yecheng Ma,
  • Yongchang Yang,
  • Xingyu Jin,
  • Tailong Yi,
  • Xianglian Ge,
  • Xing Xu,
  • Xuejun Yang,
  • Qiang Huang,
  • Yalin Lu,
  • Peng Li,
  • Wenliang Li,
  • Xiaoguang Wang,
  • Yingzhe Piao,
  • Xun Jin

摘要

G protein-coupled receptors (GPCRs) play a pivotal role in maintaining the stemness of both normal and cancer stem cells. However, the function of the regulator of G protein signaling (RGS) family, particularly in tumor stem cells, remains poorly under-stood. Through bioinformatics analysis of clinical data, we identified RGS20 as a potential regulator of glioma stemness and temozolomide (TMZ) resistance, which may significantly influence patient prognosis. Subsequent in vitro and in vivo experiments demonstrated that RGS20 inhibition markedly enhanced tumor sphere formation and upregulated stem cell markers by intrinsically activating the WNT/β-catenin signaling pathway, thereby promoting tumorigenesis and ultimately leading to TMZ resistance. Furthermore, in human glioblastoma specimens, β-catenin signaling associated with low RGS20 expression was significantly enriched in hypoxic regions, suggesting that this mechanism may support the maintenance of glioma stem cells (GSCs) and drive TMZ resistance within the hypoxic niche. Our findings reveal that low RGS20 expression sustains WNT/β-catenin signaling in a ligand-reduced manner within hypoxic niches, unveiling a novel intracellular mechanism that drives glioma progression. Targeting this mechanism could provide new therapeutic strategies for glioma treatment.