通过调节miR-361-3p/DUSP2轴,Circ-EIF3I促进肝细胞癌的进展
Lingna Ni1, Qianqian Gao2, Qiu Zhao1
1Department of Oncology, Changzhou Tumor Hospital, Changzhou, China.
DNA and cell biology
|March 21, 2024
概括
循环RNAcirc-EIF3I促进肝细胞癌 (HCC) 的进展. 下调circ-EIF3I通过miR-361-3p/DUSP2轴抑制HCC细胞的增殖和转移.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 基因规则 基因规则
背景情况:
- 肝细胞癌 (HCC) 是一种普遍存在的全球性恶性瘤.
- 循环RNAs (circRNAs) 越来越多地被认为是它们在癌症发展中的作用.
- 在HCC中circ-EIF3I的特定功能和调控机制在很大程度上是未知的.
研究的目的:
- 研究circ-EIF3I在肝细胞癌 (HCC) 进展中的生物学作用和潜在的分子机制.
- 确定下游目标和监管途径受到circ-EIF3I在HCC.影响.
主要方法:
- 使用了生物信息学分析, luciferase 记者测定,Transwell 迁移测定,细胞计数工具包-8 (CCK-8) 和5-乙烯基-2'-脱氧氨 (EdU) 测定.
- 为了验证这些发现,进行了体内瘤发生和转移试验.
- 分析了circ-EIF3I,miR-361-3p和双特异性酸酶2 (DUSP2) 的表达水平.
主要成果:
- 在HCC细胞系中,Circ-EIF3I表达显著上调.
- 低调circ-EIF3I显著抑制了hcc细胞的增殖和迁移在体外和体内.
- 生物信息学和光酶分析证实miR-361-3p和DUSP2是circ-EIF3I的直接下游目标.
- 恢复DUSP2表达或抑制miR-361-3p可以逆转circ-EIF3I降调对HCC细胞的抑制作用.
结论:
- 循环-EIF3I通过海绵 miR-361-3p 并随后调节 DUSP2.2,促进 HCC 的进展.
- 针对circ-EIF3I/miR-361-3p/DUSP2轴是一个潜在的治疗策略.
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