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在甲状腺癌中,RNF115通过调节CDK10降解来加剧瘤的进展
Jinxiang Zhu1,2, Longwei Guo3, Hao Dai1
1Department of Otorhinolaryngology-Head and Neck Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Western Yanta Road, Xi'an City, 710061, Shaanxi Province, China.
Cell biology and toxicology
|February 20, 2024
概括
戒指蛋白115 (RNF115) 通过降解CDK10促进甲状腺癌 (THCA) 的进展和转移. 这种E3酶激活了Raf-1通路,驱动THCA中的癌细胞增殖和细胞周期推进.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 戒指蛋白115 (RNF115) 是一种E3结合酶,与瘤发生和转移有关.
- 它在甲状腺癌 (THCA) 进展中的特定作用和机制尚未完全阐明.
研究的目的:
- 研究RNF115在THCA的发展中的功能和机制.
- 识别THCA中RNF115调节的下游目标和信号通路.
主要方法:
- 在THCA中使用TCGA数据库进行RNF115表达分析.
- 在体外和体内实验中评估RNF115对THCA进展的影响.
- 生物信息学分析以确定RNF115调节的蛋白质和途径.
主要成果:
- 在THCA组织和细胞中,RNF115的表达被上调.
- 升高的RNF115促进THCA细胞增殖,瘤生长,上皮-介质细胞过渡 (EMT) 和肺转移.
- CDK10被确定为下游标,被RNF115无处不在并降解,抵消RNF115的前瘤性作用.
- RNF115激活了Raf-1通路,并通过CDK10降解增强了细胞周期的进展.
结论:
- RNF115通过无处不在和降解CDK10.0驱动THCA增殖,EMT和转移.
- 这种机制涉及Raf-1通路的激活和THCA中细胞周期进展的改变.
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