热冲击因子蛋白4甲基化与结直肠癌风险以及潜在的分子机制之间的关联:生物信息学研究
Wen-Jing Zhang1, Ke-Lin Yue2, Jing-Zhai Wang2
1Department of Medical Oncology, The First People's Hospital of Yunnan Province, Affiliated Hospital of Kunming University of Science and Technology, Kunming 650032, Yunnan Province, China.
World journal of gastrointestinal oncology
|January 4, 2024
概括
热冲击因子蛋白4 (HSF4) 在结直肠癌 (CRC) 中高度甲基化,但这种甲基化与患者的预后或诊断没有显著的相关性. HSF4甲基化可能是HSF4影响CRC进展的机制.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
背景情况:
- 热冲击因子蛋白4 (HSF4) 与结直肠癌 (CRC) 的进展有关.
- 基因甲基化是影响基因表达和癌症发展稳定的关键表观遗传机制.
研究的目的:
- 为了检查HSF4DNA甲基化和CRC风险之间的关系.
- 阐明CRC中HSF4甲基化背后的分子机制.
主要方法:
- 使用闪亮的甲基化分析资源工具分析了HSF4甲基化位点及其与HSF4mRNA表达的相关性.
- 通过LinkedOmics在CRC中识别了与HSF4甲基化相关的基因,随后进行了基因本体学和基因和基因组丰富分析的京都百科全书.
- 使用String数据库和MCODE算法构建了HSF4甲基化相关基因的蛋白质-蛋白质相互作用网络.
主要成果:
- 在HSF4中确定了19个CpG甲基化位点,在CRC组织中甲基化显著增加,与HSF4mRNA表达正相关.
- 在CRC患者中发现这些HSF4 CpG位点的预后和诊断性能平.
- 在CRC中发现了1694个与HSF4甲基化相关的基因,参与免疫,炎症和代谢重编程,其中EGFR,RELA和STAT3被确定为枢纽基因.
结论:
- HSF4在CRC中表现出高甲基化,尽管与预后或诊断没有显著的相关性.
- 建议HSF4甲基化是HSF4促进CRC进展的机制.
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