MiR-183-5p通过向TET1促进细胞癌转移
Shengnan Jin1,2, Lu Chen3, Jiayi Wu1,2
1Institute of Drug Metabolism and Pharmaceutical Analysis, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
International journal of immunopathology and pharmacology
|August 16, 2023
概括
这项研究表明,miR-183-5p通过降低十-十一转位1 (TET1) 表达的调节来促进细胞癌 (RCC) 的进展. 这导致RCC的细胞入侵和迁移增加.
科学领域:
- 分子生物学分子生物学
- 在瘤学瘤学.
- 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:
- 十一转位1 (TET1) 是一种DNA脱甲基酶,对基因组甲基化调节至关重要.
- TET1失调与细胞癌 (RCC) 的进展有关,但其下调机制尚不清楚.
- 微RNA-183-5p (miR-183-5p) 是一种在各种瘤中升调的瘤基因.
研究的目的:
- 阐明RCC中TET1下调的机制.
- 研究miR-183-5p在RCC中调节TET1表达中的作用.
- 探索miR-183-5p/TET1轴对RCC细胞行为的功能后果.
主要方法:
- 细胞入侵和迁移分析 (Transwell,伤口愈合).
- 基因甲基化分析 (对TET1活性进行点滴).
- 双露西法酶记者测定证实miR-183-5p与TET1 3'-UTR结合.
主要成果:
- miR-183-5p通过与其3'-UTR结合,直接抑制RCC中的TET1表达.
- 在RCC标本中,TET1表达和5-基甲基细胞蛋白 (5hmC) 水平显著下降.
- 通过miR-183-5p对TET1的下调抑制miR-200c的表达,并促进RCC细胞的入侵和迁移.
结论:
- miR-183-5p通过向TET1.1,在RCC中起到瘤基因的作用.
- 该miR-183-5p/TET1通路影响表观遗传调节,并促进RCC细胞的攻击性.
- 针对miR-183-5p/TET1轴可能为RCC提供治疗策略.
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