USP7通过duebiquitination对MYO6进行上调,加速结直肠癌的进展
1Department of Gastrointestinal Hernia Surgery, People's Hospital of Guang'an City, Guang'an City, Sichuan 638000, China.
Mutation research
|May 30, 2025
概括
乌比基特异性蛋白酶7 (USP7) 通过去除乌比基的修饰来稳定结直肠癌 (CRC) 中的Myosin VI (MYO6). 这种相互作用促进CRC细胞生长和M2巨细胞两极分化,表明新的治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 乌比基特异蛋白酶7 (USP7) 是一种调节癌细胞过程的二维基基酶.
- 肌蛋白VI (MYO6) 在癌症中表达高,与瘤进展有关.
- USP7和MYO6都与结直肠癌 (CRC) 的进展有关.
研究的目的:
- 在CRC中调查MYO6和USP7之间的相互作用.
- 为了确定它们的相互作用是否与deubiquitination有关.
- 阐明USP7介导的MYO6二维基化在CRC中的作用.
主要方法:
- 定量实时PCR和西布洛特用于基因和蛋白质表达.
- 在体外测试 (增殖,迁移,入侵,亡) 和体内异种移植模型.
- 流细胞测量用于M2巨分离,染色质免疫沉用于蛋白质相互作用,以及用于二维化的泛化试验.
主要成果:
- 在CRC组织和细胞中高MYO6表达;MYO6沉默抑制了CRC进展和M2巨细胞两极分化.
- USP7通过二化稳定和上调MYO6,在CRC中USP7的表达高.
- USP7沉默抑制了CRC表型和M2极化,MYO6过度表达逆转了效应.
结论:
- MYO6通过USP7诱导的二维化促进CRC瘤发生和M2巨分离.
- 通过USP7介导的MYO6二基化是CRC进展的关键机制.
- 这些发现表明USP7和MYO6是基于表观遗传的CRC治疗的潜在点.
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