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长非编码RNAVPS9D1-AS1通过调节VEGFA信号通路来促进结直肠癌中的血管生成

Zheying Zhang¹, Yifei Han¹, Yang Yang¹

¹Department of Pathology, Xinxiang Medical University Xinxiang 453003, Henan, China.

American journal of cancer research

|May 15, 2025

概括

长非编码RNAVPS9D1-AS1通过上调VEGFA和激活PI3K/AKT通路促进结直肠癌 (CRC) 血管生成. 这个过程是由转录因子CEBPB启动的,突出显示VPS9D1-AS1是CRC中的关键调节者.

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:

结肠直肠癌 (CRC) 是一个主要的全球健康问题.
血管新生在CRC进展和转移中发挥着关键作用.
长非编码RNAs (lncRNAs) 越来越多地被认为是癌症的关键调节者.

研究的目的:

阐明 lncRNA VPS9D1-AS1 影响结肠直肠癌血管生成的机制.
研究VPS9D1-AS1,VEGFA和CRC中的PI3K/AKT通路之间的调控关系.
在结直肠癌的背景下,确定VPS9D1-AS1的上游调节者.

主要方法:

定量实时PCR (qRT-PCR) 和西布洛特用于评估VPS9D1-AS1表达.
基于细胞的测试 (增殖,迁移,入侵,体外管形成) 使用人类静脉内皮细胞 (HUVEC).
染色体免疫沉 (ChIP) 和双化酶记者测试以确定转录因子的结合和活性.

主要成果:

发现VPS9D1-AS1在结直肠癌组织中表达高.
与VPS9D1-AS1的干扰抑制了HUVEC的扩散,迁移和入侵.
VPS9D1-AS1通过上调VEGFA和激活PI3K/AKT通路来促进血管生成.
转录因子CEBPB直接与VPS9D1-AS1的促进子区域结合,从而增强其转录.

结论:

VPS9D1-AS1通过促进血管生成,在结直肠癌中起到关键的瘤性 lncRNA 的作用.
CEBPB是VPS9D1-AS1的上游激活剂,有助于其亲血管功能.
VPS9D1-AS1代表了抑制结直肠癌血管生成的潜在治疗标.

关键词:

在CEBPBP的基础上,CEBPBP 结肠直肠癌是一种癌症.在VEGFA中,VEGFA是VEGFA.在VPS9D1-AS1中使用VPS9D1.血管新生是因为血管新生.

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