激活ERβ的LINC01018通过调节CDC25C/CDK1/CyclinB1通路来促进子宫内膜异位症的发展
Ruihui Lu1, Jingwen Zhu1, Xin Li1
1Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing 100034, China.
Journal of genetics and genomics = Yi chuan xue bao
|January 15, 2024
概括
雌激素受体β (ERβ) 通过激活LINC01018驱动子宫内膜异位症,从而促进细胞增殖. 准这种ERβ/LINC01018通路为子宫内膜异位症提供了潜在的非激素治疗方法.
科学领域:
- 生殖生物学 生殖生物学
- 分子内分泌学分子内分泌学
- RNA生物学的RNA生物学
背景情况:
- 子宫内膜异位症是一种依赖雌激素的疾病,其中雌激素受体β (ERβ) 起着关键作用.
- 由于ERβ的广泛分布,目前针对ERβ的治疗缺乏特异性.
- 长非编码RNAs (lncRNAs) 正在成为子宫内膜异位症发病的潜在因素.
研究的目的:
- 阐明ERβ在子宫内膜异位症中的下游调节机制.
- 研究长跨基因非编码RNA 1018 (LINC01018) 作为子宫内膜异位症潜在的非激素治疗点的作用.
主要方法:
- 定量实时PCR测量ESR2和LINC01018的表达.
- 染色体免疫沉测试以评估ERβ与LINC01018促进体的结合.
- 在体外细胞培养和体内动物模型中评估LINC01018.8.的功能影响.
- 西部涂抹用于分析CDC25C/CDK1/CyclinB1通路.
主要成果:
- 在异位子宫内膜组织中,ESR2和LINC01018表达都升高,它们之间存在正相关性.
- ERβ直接与LINC01018促进子结合,激活其转录.
- 通过调节CDC25C/CDK1/CyclinB1通路,ERβ通过LINC01018促进宫外子宫内膜层细胞的增殖.
- LINC01018 knockdown 在体内显著抑制了子宫内膜病变的扩散.
结论:
- 这项研究确定了一种新的ERβ/LINC01018/CDC25C/CDK1/CyclinB1信号轴,该轴对子宫内膜异位症的进展至关重要.
- LINC01018 是一种有前途的非激素治疗点,用于经由ERβ.介导的子宫内膜异位症.
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