通过miR-152-3p下调的UBES2S通过PTEN介导的AKT/mTOR通路促进前列腺癌的进展
Chunhui Wang1,2, Gang Zhang3, Ying Jiang4
1Departments of Urology, Affiliated Hospital of Chifeng University, No. 42 Wangfu Street, 024000, Chifeng, China.
Human molecular genetics
|January 14, 2025
概括
UBE2S通过通过AKT/mTOR途径降解PTEN促进前列腺癌 (PCa) 的进展. 这个过程是由miR-152-3p调节的,这表明UBE2S是PCa的潜在诊断标记物和治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 前列腺癌 (PCa) 发病率和死亡率仍然很高,瘤发展的机制尚不清楚.
- 在PCa病变发生过程中,UBE2S的特定作用和调节尚未完全阐明.
研究的目的:
- 研究UBE2S在前列腺癌中的表达和功能.
- 阐明PCa中UBE2S的上游监管机制.
- 探索UBE2S介导的PCa进展中涉及的分子途径.
主要方法:
- 对UBE2S表达和临床相关性进行公共数据库的生物信息分析.
- 试验室试验评估UBE2S对PCa细胞增殖和侵入的影响.
- 路西法雷斯记者分析证实miR-152-3p与UBES2S结合.
- 双重免疫光和共免疫沉试验用于研究UBE2S-PTEN相互作用.
- 在裸体小鼠中进行救援实验和体内研究.
主要成果:
- UBE2S表达在PCa上调,与更高的格里森得分,高级TNM阶段,增加的生化复发和较差的无疾病生存率相关.
- miR-152-3p直接准UBE2S mRNA 3'-UTR,降低其在PCa中的表达.
- UBE2S通过ubiquitinating和降解PTEN促进PCa的进展,从而激活AKT/mTOR信号通路.
结论:
- 通过miR-152-3p负调节的UBE2S,通过PTEN/AKT/mTOR途径显著促进前列腺癌的发病和进展.
- UBE2S代表了一种潜在的新型诊断生物标志物和前列腺癌的治疗点.
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