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CLOCK通过乙化PRPS1/2促进质母细胞细胞的增殖

Juanjuan Liu¹, Zhaoyuan Meng², Runze Wang¹

¹Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao Cancer Institute, School of Basic Medicine of Qingdao University, Qingdao, 266000, China.

Journal of neuro-oncology

|July 19, 2025

概括

皮表皮生长因子 (EGF) 激活了一条涉及CK2,CLOCK和PRPS1/2的途径,破坏昼夜节律并促进质母细胞瘤 (GBM) 的生长. 这种EGFR-CLOCK-PRPS1/2轴与侵袭性瘤和患者生存率低下有关.

科学领域:

分子生物学分子生物学
癌症研究癌症研究
时间生物学时间生物学

背景情况:

循环时钟功能障碍与癌症的发展有关.
皮表皮生长因子受体 (EGFR) 的激活对于质母细胞瘤 (GBM) 发病过程至关重要.
在GBM中,EGFR信号与生理时钟调节之间的联系在很大程度上仍未被探索.

研究的目的:

调查EGFR激活是否影响GBM的昼夜时钟.
阐明EGFR信号通过昼夜钟影响GBM瘤发生的分子机制.
在EGFR-CLOCK-PRPS1/2轴内识别潜在的治疗点.

主要方法:

利用分子生物学技术,包括DNA突变,qPCR,免疫沉和免疫光.
产生了CLOCK和PRPS1/2突变体,并使用了shRNA用于基因沉默.
评估了GBM细胞的增殖和迁移,并分析了GBM标本中的蛋白质表达和局部化.

主要成果:

EGF刺激导致S106的CK2介导的CLOCK酸化,破坏了CLOCK-BMAL1结合和昼夜基因表达.
酸化的CLOCK被从核中输出,导致PRPS1/2.2.的细胞酸性乙化.
这种乙化稳定了PRPS1/2,增强了GBM细胞的增殖和迁移;高水平的CLOCK pS106,PRPS1/2 K29ac和PRPS1/2与晚期瘤阶段和低生存率相关.

结论:

EGFR激活通过通过CLOCK酸化和随后的PRPS1/2乙化来破坏昼夜节律,促进GBM的进展.
已确定的EGFR-CLOCK-PRPS1/2轴代表了GBM中一种新的致癌途径.
临床发现表明,CLOCK pS106,PRPS1/2 K29ac和PRPS1/2是侵略性GBM和不良预后的潜在生物标志物.

关键词:

乙化乙化是一种钟表的时间欧洲农业基金会 (EGFR) 是一个基金.在GBMGBMGBMGBMGBM 在PRPS1/2中.酸化是指酸化的方法.

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