MicroRNA-340 inhibits the proliferation and invasion of hepatocellular carcinoma cells by targeting JAK1
- The 5th Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai (China)
- The 2nd Department of Special Treatment, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai (China)
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. - Highlights: • miR-340 is downregulated in HCC and suppresses HCC cell proliferation, migration, and invasion. • miR-340 overexpression on HCC xenograft tumor growth in nude mice. • miR-340 directly targets JAK1. • miR-340 regulates the JAK1/STAT3 signaling pathway.
- OSTI ID:
- 22696840
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 483, Issue 1; Other Information: Copyright (c) 2016 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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