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在肺腺癌中,O-GlcNAcylation驱动的TR11B生产和功能的病理作用

Shiyu Qiu¹, Lifang Ma², Keke Yu³

¹Department of Clinical Laboratory, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China; Shanghai Institute of Thoracic Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China.

Developmental cell

|September 10, 2025

概括

瘤坏死因子受体超级家族11B成员 (TR11B) 驱动肺腺癌 (LUAD) 的进展和抵抗. O-GlcNAcylation稳定了TR11B,为LUAD治疗提供了一个新的治疗点.

科学领域:

生物化学生物化学
分子生物学分子生物学
在瘤学瘤学.

背景情况:

细胞因子与炎症和瘤发生有关.
在瘤微环境中的细胞因子功能转化后修改的作用尚不清楚.

研究的目的:

研究瘤衍生性瘤缩因子 (TNF) 受体超级家族11B成员 (TR11B) 在肺腺癌 (LUAD) 进展和治疗耐药性中的作用.
通过翻译后修改,特别是O-GlcNAcylation,阐明TR11B调节的机制.

主要方法:

确定TR11B是LUAD中的一个关键驱动因素.
涉及O-GlcNAc转移酶 (OGT),O-GlcNAcylation以及与EPS15同源域含蛋白1 (EHD1) 的相互作用的机制研究.
对循环林依赖激酶2 (CDK2) 酸化和细胞循环进展的分析.
O-GlcNAcylated TR11B水平与LUAD阶段的临床相关性.
在LUAD小鼠模型中评估Ogt的遗传删除.
评估赛莱科西布对O-GlcNAcylation和瘤生长的影响.

主要成果:

来自瘤的TR11B促进LUAD的进展和治疗耐药性.
在血清151的O-GlcNAcylation稳定TR11B,并增强其与EHD1的相互作用,从而导致CDK2酸化和细胞循环促进.
升高的O-GlcNAcylated TR11B水平与高级的LUAD相关.
在小鼠模型中,Ogt的遗传删除抑制了LUAD的发展.
切莱科克西布抑制O-GlcNAcylation,并在LUAD中显示出抗瘤作用.

结论:

TR11B的O-GlcNAcylation是推动LUAD进展和治疗耐药性的关键机制.
OGT-TR11B轴代表了LUAD的潜在治疗目标.
塞莱科克西布通过准这种途径显示出作为治疗剂的希望.

关键词:

这是一种O-GlcNAcylation.细胞循环中的细胞循环.细胞因子细胞因子肺部腺癌的癌症.瘤发生的起源

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