长非编码RNA RHPN1-AS1通过与RPS15A蛋白相互作用,在缺氧下促进肝细胞癌的进展
Qin Peng1,2, Yu-Ting Cai1,2, Qi Ding1,2
1Ward II, Department of Gastrointestinal Oncology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No.107 Huanhu East Road, Shushan District, Hefei, 230031, China.
Medical oncology (Northwood, London, England)
|September 30, 2025
概括
缺氧会增加肝癌细胞中的RHPN1-AS1长非编码RNA,通过稳定RPS15A蛋白和激活β-catenin通路来促进瘤生长. 这突出了RHPN1-AS1作为低氧性肝细胞癌的治疗点.
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:
- 缺氧是肝细胞癌 (HCC) 的一个关键特征,推动癌症的进展.
- 像RHPN1-AS1这样的长非编码RNA (lncRNAs) 与各种癌症有关,但它们在缺氧HCC中的作用尚不清楚.
研究的目的:
- 在低氧条件下研究HCC中的RHPN1-AS1表达和功能.
- 在低氧性HCC中确定RHPN1-AS1的蛋白伴侣和分子机制.
主要方法:
- 研究了暴露于缺氧的HCC细胞中的RHPN1-AS1表达变化.
- 进行了RHPN1-AS1.1.的淘汰和过度表达研究.
- 使用了染色体免疫沉降和蛋白质相互作用测试.
- 在异种移植模型中进行了体内瘤原性研究.
主要成果:
- 缺氧增加了RHPN1-AS1水平,由HIF-1α调节.
- 抑制RHPN1-AS1突击,同时促进过度表达,在低氧状态下促进HCC细胞的增殖和入侵.
- RHPN1-AS1稳定了RPS15A蛋白,通过β-catenin信号增强了HCC细胞的攻击性.
- 在体内,RPS15A的减少减少了瘤的生长.
结论:
- RHPN1-AS1 是 HCC 中的低氧反应性 lncRNA.
- 通过与RPS15A相互作用并激活β-catenin通路,RHPN1-AS1促进了HCC的进展.
- RHPN1-AS1和RPS15A代表了低氧HCC的潜在治疗点.
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