通过准miR-497-5p/SPP1轴,LncRNA TRPM2-AS促进子宫内膜癌的进展和血管生成
Hanbo Ma1,2,3, Fengyun Weng4, Xiaowen Tong3
1Department of Obstetrics and Gynecology, International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, China.
Cellular & molecular biology letters
|July 3, 2024
概括
长非编码RNATRPM2-AS通过海绵miR-497-5p增加SPP1.1,促进内皮癌 (EC) 的生长和血管生成. 削弱TRPM2-AS抑制了EC致癌性,提供了一个新的治疗点.
科学领域:
- 分子瘤学分子瘤学
- 癌症生物学 癌症生物学
- 血管新生研究研究
背景情况:
- 抗血管生成疗法是瘤的关键治疗方法.
- 长非编码RNAs (lncRNAs) 调节内皮癌 (EC) 的瘤发生和血管发生.
- 在EC中lncRNA TRPM2-AS的具体作用尚不清楚.
研究的目的:
- 研究lncRNA TRPM2-AS在EC中的作用和机制.
- 探索TRPM2-AS作为EC治疗的潜在治疗点.
主要方法:
- 生物信息分析以确定预后 lncRNAs 并构建一个 ceRNA 网络.
- 实验验证包括FISH,基于细胞的试验 (CCK-8,EdU,transwell),qRT-PCR,西斑和内皮管形成试验.
- 在体内研究使用皮下瘤模型和瘤免疫微环境的分析.
主要成果:
- 在欧共体中,TRPM2-AS和SPP1被上调,而miR-497-5p被下调.
- TRPM2-AS通过菌miR-497-5p促进EC细胞的增殖,入侵,迁移和血管生成,从而导致SPP1释放.
- 在体内,TRPM2-AS knockdown 抑制了瘤生长和血管生成,并调节了瘤免疫微环境.
结论:
- TRPM2-AS通过miR-497-5p/SPP1轴促进了EC的致癌性.
- TRPM2-AS在EC血管生成和免疫微环境调节中发挥着重要作用.
- TRPM2-AS代表了EC治疗的新型治疗点.
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