通过生物信息学分析在慢性髓性白血病细胞中识别与ubiquitination相关的枢纽基因
Qian Zhou1,2,3, Zhuoran Li1,2,3, Li Meng1,2,3
1Key Lab of Chemical Biology (MOE), School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China.
Journal of Cancer
|June 24, 2024
概括
这项研究确定了UHRF1和CDC20作为慢性髓性白血病干细胞 (CML-LSCs) 中关键的泛化相关基因. 向这些基因可能会提供一种新的策略来根除CML-LSCs并克服治疗耐药性.
科学领域:
- 血液学 血液学 血液学
- 在瘤学瘤学.
- 分子生物学分子生物学
背景情况:
- 慢性髓性白血病干细胞 (CML-LSCs) 驱动TKI耐药性和CML复发.
- 乌比基化与CML进展有关,但其在CML-LSCs中的特定作用需要进一步阐明.
研究的目的:
- 通过生物信息学分析,识别CML-LSC中潜在的随处可见相关基因.
- 探索这些基因作为消除CML-LSCs的治疗点.
主要方法:
- 在正常HSC和CML-LSC之间对与ubiquitination相关的基因的差异基因表达分析.
- 蛋白质与蛋白质相互作用网络分析以确定枢纽基因.
- 对上游监管网络 (转录因子和微RNA) 的分析.
- 与免疫细胞透的相关性分析和CML模型中的功能验证.
主要成果:
- 确定了四个与枢纽无处不在相关的基因 (AURKA,Fancd2,Cdc20, Uhrf1) 并与LCS中的免疫细胞透有关.
- 发现UHRF1和CDC20在CML-LSCs中高度表达.
- 抑制Fancd2,Cdc20和Uhrf1显著抑制了CML细胞的扩散.
结论:
- UHRF1和CDC20是CML-LSCs中新的关键无化相关基因.
- 这些基因在CML的发病过程中发挥着重要作用.
- 准UHRF1和CDC20为CML提供了一个潜在的治疗策略.
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