Here, we aim to explore whether tribbles pseudokinase 3 (TRIB3) enhances glioma cell stemness. TRIB3 was overexpressed in glioma tissues and cell‐formed spheres, positively correlated with the size and grade. Additionally, TRIB3 expression displayed a negative correlation with the overall survival rate of glioma patients. Moreover, TRIB3 knockdown reduced the stemness of nonadherent spheres, evident by the decreased sphere‐forming ability, stemness master expression, and ALDH1 activity, while TRIB3 overexpression enhanced the stemness of adherent cells, which was rescued by β‐catenin knockdown. Mechanistically, TRIB3 activated β‐catenin signaling via physically interacting with β‐catenin. This study suggests that the TRIB3‐β‐catenin interaction is responsible for glioma cell stemness.

中文翻译：

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TRIB3 通过与 β-catenin 相互作用赋予胶质瘤细胞干性

在这里，我们旨在探索 Tribbles 假激酶 3 (TRIB3) 是否增强神经胶质瘤细胞干性。TRIB3在胶质瘤组织和细胞形成的球体中过度表达，与大小和等级呈正相关。此外，TRIB3 表达与胶质瘤患者的总生存率呈负相关。此外，TRIB3 敲低降低了非粘附球的干性，这表现为球形成能力、干性主表达和 ALDH1 活性的降低，而 TRIB3 过表达增强了贴壁细胞的干性，β-连环蛋白敲低可以挽救这种干性。从机制上讲，TRIB3 通过与 β-catenin 的物理相互作用激活 β-catenin 信号传导。该研究表明 TRIB3-β-catenin 相互作用是神经胶质瘤细胞干性的原因。