长非编码RNA VCAN-AS1通过HuR/F11R通路促进胃癌的进展
Wei Xu1, Hao Zuo1, Xinsheng Miao1
1Department of Gastrointestinal Surgery, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University Suzhou 215002, Jiangsu, China.
American journal of translational research
|December 16, 2024
概括
长非编码RNA VCAN反感RNA 1 (VCAN-AS1) 通过与HuR相互作用来调节F11R表达,促进胃癌 (GC) 的进展. 这种VCAN-AS1/HuR/F11R通路为GC提供了潜在的治疗标.
科学领域:
- 分子瘤学分子瘤学
- RNA生物学的RNA生物学
- 癌症遗传学 癌症遗传学
背景情况:
- 胃癌 (GC) 仍然是一个重要的全球健康挑战,具有复杂的分子基础.
- 长非编码RNAs (lncRNAs) 越来越多地被认为是它们在癌症发育和进展中的作用.
- 了解像VCAN-AS1这样的lncRNAs的特定功能和相互作用,对于确定新的治疗策略至关重要.
研究的目的:
- 研究VCAN反感RNA1 (VCAN-AS1) 在胃癌 (GC) 进展中的作用.
- 阐明VCAN-AS1影响GC的分子机制,重点关注其与ELAV类RNA结合蛋白1 (HuR) 的相互作用.
- 确定VCAN-AS1/HuR相互作用对GC中的F11受体 (F11R) 表达的作用.
主要方法:
- 使用RT-qPCR对GC组织和细胞系中的VCAN-AS1表达的量化.
- 在体外和体外功能测试 (CCK-8,殖民地形成,Transwell迁移,异种移植模型) 来评估VCAN-AS1对GC细胞行为的影响.
- RNA免疫沉 (RIP) 和RNA下拉试验证实了VCAN-AS1和HuR之间的直接相互作用.
主要成果:
- 在GC组织和细胞系中,VCAN-AS1表达显著上调,与患者预后较差相关.
- 抑制VCAN-AS1可以抑制GC细胞的增殖和迁移.
- VCAN-AS1与HuR直接相互作用,这种相互作用调节F11R表达的调节,有助于VCAN-AS1在GC中的致癌作用.
结论:
- 通过HuR/F11R通路,VCAN-AS1促进了GC的进展.
- 这项研究为GC的病变产生提供了新的见解.
- VCAN-AS1成为胃癌治疗的潜在治疗标.
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