TET3介导的DNA脱甲基化修饰激活SHP2表达,通过EGFR/ERK通路促进子宫内膜癌的进展
Fen Xue1,2, Lifen Liu1, Xueqiang Tao3
1Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Journal of gynecologic oncology
|March 8, 2024
概括
十-十一转位3 (TET3) 通过DNA脱甲基化在子宫内膜癌 (EC) 中激活Src同型型酸酶2 (SHP2),通过EGFR/ERK通路促进瘤生长.
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:
- 子宫内膜癌 (EC) 的进展与Src同类型的氨酸酸酶2 (SHP2) 有关,但其在EC中的特定作用和调控机制尚未完全理解.
- 调查SHP2的上游调节者对于理解EC病原性至关重要.
研究的目的:
- 阐明十-十一转位3 (TET3) 在调节SHP2表达及其在子宫内膜癌 (EC) 中的致癌功能的作用.
- 探索TET3影响SHP2活动和EC下游信号通路的分子机制.
主要方法:
- 来自EC和对照组织的转录基因数据的生物信息分析.
- 在体外研究涉及基因淘汰 (SHP2,TET3) 和过度表达,细胞增殖,迁移和入侵分析.
- 在小鼠体内瘤异种移植模型中,以评估瘤发生能力.
主要成果:
- 发现TET3和SHP2在EC组织中过度表达.
- TET3直接与SHP2促进体结合,增强DNA基甲基化和激活SHP2.
- 通过TET3激活SHP2,促进表皮生长因子受体 (EGFR) /细胞外信号调节激酶 (ERK) 途径,驱动EC细胞的攻击性和瘤发生.
结论:
- TET3通过促进SHP2促进者的DNA脱甲基化,从而导致SHP2激活,在EC中起到瘤基因的作用.
- TET3-SHP2轴通过EGFR/ERK信号通路驱动EC的进展.
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