癌症研究
车站3
STAT蛋白
小RNA
异位表达
细胞生长
癌变
细胞周期蛋白E1
细胞周期蛋白D1
贾纳斯激酶
生物
信号转导
细胞培养
化学
细胞
细胞生物学
细胞周期
癌症
基因
生物化学
遗传学
作者
Jianyong Yuan,Hongxiang Ji,Feng Xiao,Zhipeng Lin,Xijun Zhao,Zhouchong Wang,Jingbo Zhao,Junhua Lü
标识
DOI:10.1016/j.bbrc.2016.12.102
摘要
Increasing evidence indicates that dysregulation of microRNAs (miRNAs) contributes to tumorigenesis. MicroRNA-340 (miR-340) is downregulated in several types of cancer. However, the functional mechanism of miR-340 in hepatocellular carcinoma (HCC) remains unclear. Here, we showed that miR-340 was significantly downregulated in HCC tissues and cell lines. Gain-of-function experiments demonstrated that miR-340 overexpression inhibited HCC cell proliferation, migration, and invasion in vitro, and suppressed tumor growth in vivo. Janus kinase 1 (JAK1) was identified as a direct target of miR-340 in HCC cells. Ectopic expression of JAK1 reversed the inhibitory effects of miR-340. Further investigations showed that miR-340 dramatically inhibited the expression of signal transducer and activator of transcription (STAT)3 downstream molecules including Bcl-2, cyclin D1, and matrix metalloprotease (MMP)-2. The present findings indicated that miR-340 suppressed HCC cell proliferation and invasion by regulating the JAK1/STAT3 pathway, suggesting its potential as a novel therapeutic target for HCC.
科研通智能强力驱动
Strongly Powered by AbleSci AI