MicroRNA-340 inhibits the proliferation and invasion of hepatocellular carcinoma cells by targeting JAK1
| Autor: | Xijun Zhao, Zhipeng Lin, Feng Xiao, Jun Zhao, Jun-Hua Lu, Zhouchong Wang, Jianyong Yuan, Hongxiang Ji |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
STAT3 Transcription Factor Carcinoma Hepatocellular Biophysics Mice Nude medicine.disease_cause Biochemistry 03 medical and health sciences Mice 0302 clinical medicine Cyclin D1 Cell Movement microRNA medicine Animals Humans Neoplasm Invasiveness STAT3 Molecular Biology Cell Proliferation Mice Inbred BALB C biology Janus kinase 1 Chemistry Cell growth Liver Neoplasms Cell Biology Hep G2 Cells Janus Kinase 1 digestive system diseases Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology HEK293 Cells 030220 oncology & carcinogenesis Immunology Cancer research STAT protein biology.protein Ectopic expression Carcinogenesis Neoplasm Transplantation Signal Transduction |
| Zdroj: | Biochemical and biophysical research communications. 483(1) |
| ISSN: | 1090-2104 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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