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通过雌激素介导的DNMT1和DNMT3A由EZH2的招募使得miR-570-3p沉默,该miR-570-3p通过DPP4促进皮质甲状腺恶性瘤
Xiarong Hu1, Qingyao Ye1, HuanQuan Lu1
1Department of General Surgery, The Tenth Affiliated Hospital of Southern Medical University (Dongguan People's Hospital), Dongguan, 523059, Guangdong, China.
Clinical epigenetics
|June 18, 2024
概括
雌激素通过通过EZH2/DNMTs通路增加miR-570-3p甲基化来促进乳头甲状腺癌 (PTC) 的生长. 这种表观遗传调节降低了miR-570-3p的调节,增强了瘤的进展.
科学领域:
- 内分泌学 在内分泌学.
- 分子生物学分子生物学
- 在瘤学瘤学.
背景情况:
- 乳头甲状腺癌 (PTC) 是一种普遍存在的内分泌恶性瘤.
- 雌激素在调节微RNAs (miRNAs) 的作用在各种癌症中得到了认可.
- 在PTC中,miR-570-3p的特定功能及其与雌激素的联系仍未得到充分研究.
研究的目的:
- 研究miR-570-3p在PTC中的调节作用.
- 在PTC中确定雌激素 (特别是雌二醇E2) 和miR-570-3p之间的直接关联.
- 阐明雌激素对miR-570-3p表达和PTC进展的影响的分子机制.
主要方法:
- 生物信息预测和qRT-PCR/西斑验证miR-570-3p和DPP4表达.
- 为了评估miR-570-3p/DPP4轴功能的体外和体内损益实验.
- 对miR-570-3p促进物甲基化 (MSP) 和EZH2/DNMTs/E2相互作用 (露西法酶,ChIP,co-IP测试) 的分析.
主要成果:
- 在PTC组织/细胞中,miR-570-3p的下调和高甲基化.
- DPP4被确定为miR-570-3p的直接标;miR-570-3p抑制了PTC细胞的增殖,迁移,入侵,并促进了细胞亡,DPP4的效应被逆转.
- 雌激素 (E2) 通过EZH2 / DNMTs增加了miR-570-3p促进剂甲基化,减少了miR-570-3p表达并促进了PTC生长.
结论:
- 雌激素通过表观遗传沉默miR-570-3p促进PTC进展.
- 通过EZH2/DNMTs途径调解雌激素诱导的miR-570-3p抑制.
- miR-570-3p/DPP4轴是由雌激素调节的PTC发育中的关键参与者.
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