期刊
SCIENTIFIC REPORTS
卷 2, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep00637
关键词
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资金
- Ministry of Education, Culture, Sports, Science and Technology, Japan [22390058, 24590956, 20390204]
- Health Sciences Research Grants of The Ministry of Health, Labour and Welfare of Japan
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Yakult Bio-Science Foundation
- Cell Science Research Foundation
- Grants-in-Aid for Scientific Research [20390204, 24590956, 22390058] Funding Source: KAKEN
Hepatitis C virus (HCV) infection is a major cause of chronic liver disease worldwide. Although novel drugs against HCV are under development, the current standard therapy consists principally of interferon (IFN). To improve the response to IFN treatment by enhancing interferon-stimulated response element (ISRE)-mediated gene transcription, we screened 75 microRNAs highly expressed in hepatocytes for their ability to modulate ISRE activity. Overexpression of microRNA-122 (miR122) significantly suppressed ISRE activity. Conversely, silencing of miR122 function enhanced IFN-induced ISRE activity, by decreasing expression of suppressor of cytokine signaling 3 (SOCS3). This decrease in SOCS3 level was not mediated by microRNA target gene suppression, but rather by enhanced methylation at SOCS3 gene promoter. Taken together, our data, along with the fact that antisense oligonucleotides of miR122 also directly inhibit HCV replication, suggest that a combination therapy comprising IFN and silencing of miR122 function may be a promising therapeutic option in the near future.
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