通过通过m6A修饰激活TRAF6/NF-κB/FGF18,BUB1增强了胃癌的扩散和转移
Kun Wang1, Kanger Shen1, Jiayu Wang2
1Jiangsu Institute of Clinical Immunology, The First Affiliated Hospital of Soochow University, Suzhou, China; Jiangsu Key Laboratory of Clinical Immunology, Soochow University, Suzhou, China; Department of Gastroenterology, the First Affiliated Hospital of Soochow University, Suzhou, China.
Life sciences
|July 18, 2024
概括
通过激活TRAF6/NF-κB/FGF18通路,BUB1促进胃癌 (GC) 的生长和扩散. 针对这种途径为GC诊断和治疗提供了一个新的策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 胃癌 (GC) 是一种流行于消化系统的恶性瘤.
- BUB1激酶与各种癌症有关,但其在GC中的作用仍未定义.
研究的目的:
- 阐明BUB1在胃癌进展中的功能和分子机制.
- 研究BUB1作为GC的潜在诊断和治疗点.
主要方法:
- 在体外和体内使用BUB1抑制剂,siRNA和过度表达等离子体的功能研究.
- 在GC组织中检测BUB1和FGF18表达的免疫组织化学 (IHC).
- 通过RNA-seq,Western blot,MeRIP-qPCR和Co-IP测试来探索分子途径.
主要成果:
- 淘汰BUB1抑制了GC细胞的增殖和转移;BUB1的过度表达促进了这些过程.
- 高的BUB1和FGF18表达与GC患者预后不佳相关.
- BUB1通过METTL3-介导的TRAF6mRNA的m6A修改激活NF-κB/FGF18轴.
结论:
- 通过METTL3-介导的m6A甲基化,BUB1通过激活TRAF6/NF-κB/FGF18通路来驱动GC增殖和转移.
- BUB1/METTL3/TRAF6/NF-κB/FGF18轴代表了GC的潜在新型诊断和治疗策略.
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