| 注册
首页|期刊导航|激光生物学报|circHIPK3通过竞争性结合miR-599调控CD276表达促进肝癌发展

circHIPK3通过竞争性结合miR-599调控CD276表达促进肝癌发展

戴一岚 欧阳密 李志伟 周号悦 蒋志翔 丁小凤 李立民

激光生物学报2025,Vol.34Issue(5):409-416,8.
激光生物学报2025,Vol.34Issue(5):409-416,8.DOI:10.3969/j.issn.1007-7146.2025.05.004

circHIPK3通过竞争性结合miR-599调控CD276表达促进肝癌发展

circHIPK3 Promotes Hepatocellular Carcinoma Development by Competitively Binding miR-599 to Regulate CD276 Expression

戴一岚 1欧阳密 1李志伟 1周号悦 1蒋志翔 2丁小凤 1李立民2

作者信息

  • 1. 湖南师范大学生命科学学院基因功能与调控实验室,长沙 410081
  • 2. 湖南师范大学工程与设计学院,长沙 410081
  • 折叠

摘要

Abstract

Hepatocellular carcinoma(HCC)is the third leading cause of cancer-related mortality worldwide,characterized by poor prognosis and a high recurrence rate.To investigate the regulatory mechanism of circHIPK3 in HCC,we analyzed the expression levels of HIPK3 and its circular RNA isoform,circHIPK3,using quantitative real-time PCR(qRT-PCR),and found both to be significantly upregulated in HCC cells.Dual-luciferase reporter assays confirmed that circHIPK3 directly binds to miR-599,and that miR-599 targets the 3'untranslated region(UTR)of CD276.Furthermore,we established a stable HCC cell line with circHIPK3 knockdown(si-circHIPK3)and transfected miR-599 mimics to assess functional consequences.The results demonstrated that circHIPK3 can act as a competing endogenous RNA(ceRNA)to sponge miR-599,thereby alleviating its inhibitory effect on CD276 and upregulating CD276 expression,and enhancing the proliferation and migration ability of HCC cells.Collectively,our findings elucidate the circHIPK3/miR-599/CD276 regulatory axis in HCC progression,providing novel molecular insights into the malignant behavior of HCC cells and highlighting a potential therapeutic target.

关键词

肝癌/环状同源域相互作用蛋白激酶/微小核糖核酸-599/分化簇276/治疗靶点

Key words

hepatocellular carcinoma/circHIPK3/miR-599/CD276/therapeutic target

分类

生物学

引用本文复制引用

戴一岚,欧阳密,李志伟,周号悦,蒋志翔,丁小凤,李立民..circHIPK3通过竞争性结合miR-599调控CD276表达促进肝癌发展[J].激光生物学报,2025,34(5):409-416,8.

基金项目

国家自然科学基金项目(81872256) (81872256)

湖南师范大学交叉学院培育团队项目(2023JC203). (2023JC203)

激光生物学报

1007-7146

访问量0
|
下载量0
段落导航相关论文