N-甲基氨酸阅读器YTHDF2介导的AC026691.1降解促进胃癌细胞的增殖,迁移和M2巨细胞的两极分化
Cong-Fei Ji1, Jin-Feng Ji2, Xiao-Bing Yu3
1Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
Molecular medicine reports
|March 7, 2025
概括
与N6-甲基氨酸 (m6A) 相关的长非编码RNAAC026691.1,由YTHDF2调节,促进胃癌的进展. 它被YTHDF2降解,增强了细胞增殖,迁移和M2巨细胞两极分化,提供了潜在的治疗点.
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:
- 胃癌 (GC) 是一个重要的全球健康问题.
- 长非编码RNAs (lncRNAs) 在癌症发展中起着至关重要的作用.
- 在癌症调控中,N6-甲基氨酸 (m6A) 修饰越来越被认可.
研究的目的:
- 研究m6A相关 lncRNAs在胃癌中的作用.
- 探索这些lncRNAs对癌细胞恶性和巨细胞两极分化的影响.
- 阐明涉及YTHDF2和AC026691.1.1.的潜在机制.
主要方法:
- 来自癌症基因组图谱 (TCGA) 的GC lncRNA数据集的生物信息分析.
- 使用Cox和拉索回归对预后m6A相关的差异表达lncRNAs (DElncRNAs) 的查.
- 通过RT-qPCR和MeRIP-qPCR验证lncRNA表达和甲基化.
- 使用RNA拉下测试对lncRNA-蛋白相互作用的研究.
- 功能性研究涉及GC细胞系中YTHDF2和AC026691.1的敲除.
主要成果:
- 与m6A相关的lncRNAAC026691.1被确定为GC的预后标志物.
- YTHDF2与AC026691.1结合,并促进其m6A介导的降解.
- 在GC细胞中,AC026691.1的表达低,而YTHDF2的表达高.
- YTHDF2敲除抑制了GC细胞的增殖,迁移,EMT和M2极化;AC026691.1敲除具有相反的效果.
结论:
- 由YTHDF2介导的m6A修饰和随后的AC026691.1降解有助于胃癌的进展.
- 这个调节轴影响细胞增殖,迁移,上皮细胞-介质细胞过渡和M2巨细胞两极分化.
- 针对YTHDF2-AC026691.1相互作用可能为胃癌提供一种新的治疗策略.
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