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通过调节Huh7细胞中的多个转录因子,USF1调节转录和细胞功能
Yan-Li Zeng1,2,3, Fei Gao1, Can Zhang1
1Department of Infectious Diseases, Henan Key Laboratory for Infectious Diseases, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.
Oncology letters
|November 29, 2023
概括
上游转录因子1 (USF1) 调节了肝癌中的许多基因. 它影响免疫反应和非编码RNA,可能会影响肝细胞癌 (HCC) 的进展,并提供新的治疗点.
科学领域:
- 分子瘤学和癌症基因组学
- 基因调节和表观遗传学
背景情况:
- 肝细胞癌 (HCC) 在全球面临着显著的死亡率和转移挑战.
- 上游转录因子1 (USF1) 在HCC病变发生中的作用及其分子点在很大程度上仍未被描述.
研究的目的:
- 研究USF1在HCC中的下游转录目标和调控功能.
- 在肝癌中识别USF1调节基因网络中的潜在治疗点.
主要方法:
- 在USF1-过度表达的Huh7细胞中通过RNA测序和染色体免疫沉 (ChIP) 测序进行全转录组分析.
- 使用逆转录定量PCR (RT-qPCR) 验证下游目标.
- 整合转录和ChIP测序数据以识别直接和间接目标.
主要成果:
- USF1显著调节350个差异表达基因 (DEGs),其中上调的基因参与免疫/炎症通路,下调的基因包括长非编码RNA (lncRNAs).
- USF1直接与2,492个基因的促进子区域结合,可能影响病毒的进展和细胞增殖.
- 整合揭示了16个重叠的基因,包括lncRNA-NEAT1和转录因子ETV5,具有不同的表达模式和与USF1.1的预后相关性.
结论:
- USF1直接与数千个基因促进体结合,并间接调节大量的DEG,特别是通过调节ETV5.5来调节.
- 下游目标如lncRNA-NEAT1和TF-ETV5在USF1介导的HCC进展中发挥着潜在的作用.
- USF1及其确定下游目标代表了未来HCC治疗策略的有希望的途径.
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