IGF2BP2 可调节自噬,是胶质瘤的预后标志物

Ibrain Pub Date : 2024-03-11 DOI:10.1002/ibra.12150
Ning Li, Limei Deng, Yuming Zhang, Xilian Tang, Bingxi Lei, Qingyu Zhang
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摘要

胶质瘤是一种源自神经胶质细胞的恶性脑肿瘤,给治疗带来了巨大挑战。然而,胶质瘤发展的内在机制尚未完全明了,也缺乏有效的靶点。本研究深入探讨了胰岛素样生长因子2信使RNA结合蛋白2(IGF2BP2)在胶质瘤发展过程中的作用及其治疗潜力。我们的分析表明,在癌症基因组图谱(TCGA)数据库中,IGF2BP2表达升高与低级别胶质瘤(LGG)患者的生存期明显缩短有关。IGF2BP2消耗会导致细胞活力受损、G0/G1期停滞和集落形成能力下降。此外,超微结构分析和mCherry-GFP-LC3报告检测显示,IGF2BP2敲除后自噬体的丰度增加。Western 印迹分析证实了这些发现,显示 IGF2BP2 敲除后 p62 水平降低,LC3-ІІ/LC3-I 比率增加。多色免疫组化分析表明,在胶质瘤患者样本中,IGF2BP2 和 p62 的表达呈正相关。此外,我们的分析表明,在TCGA-LGG样本中,IGF2BP2的表达与耐药标记物之间存在联系,细胞计数试剂盒-8细胞活力测定显示,敲除IGF2BP2可使细胞对替莫唑胺治疗敏感。这一全面探索揭示了IGF2BP2在胶质瘤进展中的作用,为胶质瘤治疗中的自噬调节和化疗增敏策略提供了启示。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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IGF2BP2 modulates autophagy and serves as a prognostic marker in glioma

Glioma, a malignant brain tumor originating from neural glial cells, presents significant treatment challenges. However, the underlying mechanisms of glioma development are not fully understood, and effective targets are lacking. This study provides insights into the role of insulin-like growth factor 2 messenger RNA-binding protein 2 (IGF2BP2) in glioma progression and its therapeutic potential. Our analysis illustrated that elevated IGF2BP2 expression associated with significantly shorter survival among patients with low-grade glioma (LGG) in The Cancer Genome Atlas (TCGA) database. IGF2BP2 depletion led to compromised cell viability, G0/G1 phase arrest, and reduced colony-formation ability. Furthermore, ultrastructural analysis and mCherry-GFP-LC3 reporter assay revealed an increased abundance of autophagosomes upon IGF2BP2 knockdown. Western blot analysis corroborated these findings by showing reduced p62 levels coupled with increased LC3-ІІ/LC3-I ratio upon IGF2BP2 knockdown. A multicolor immunohistochemistry assay demonstrated the positive correlation between IGF2BP2 and p62 expression in glioma patient samples. Additionally, our analysis suggested a link between IGF2BP2 expression and drug-resistant markers in TCGA-LGG samples, and Cell Counting Kit-8 cell viability assay revealed that knockdown of IGF2BP2 sensitized cells to temozolomide treatment. This comprehensive exploration unveils the role of IGF2BP2 in glioma progression, shedding light on autophagy modulation and chemosensitization strategies for glioma therapy.

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