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c‐Myc‐mediated overexpression of miR‐17‐92 suppresses replication of hepatitis B virus in human hepatoma cells
Author(s) -
Jung Yong Jin,
Kim JinWook,
Park Soo Jin,
Min Bo Young,
Jang Eun Sun,
Kim Nam Young,
Jeong SookHyang,
Shin Cheol Min,
Lee Sang Hyub,
Park Young Soo,
Hwang JinHyeok,
Kim Nayoung,
Lee Dong Ho
Publication year - 2013
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.23534
Subject(s) - hepatitis b virus , gene knockdown , virology , microrna , viral replication , biology , hepatitis b virus pre beta , virus , rna interference , gene , microbiology and biotechnology , reporter gene , gene expression , rna , genetics , hepatitis b virus dna polymerase
MicroRNAs (miRNAs) regulate post‐transcriptional gene expression in various physiological and pathological processes, including viral infections. The miR‐17‐92 cluster encodes six miRNAs (miR‐17‐5p, miR‐18a, miR‐19a, miR‐19b, miR‐20a, and miR‐92a‐1) which are transactivated by c‐Myc. Because hepatitis B virus transactivates c‐Myc, the interaction between the miR‐17‐92 cluster and HBV replication was examined in this study. Inducing HBV replication in a human hepatoma cell line increased miR‐17‐5p, miR‐20a and miR‐92a‐1 expression. HBV‐induced overexpression of miR‐17‐92 was reversed by c‐Myc knockdown. Antisense peptide nucleic acids against miR‐20a and miR‐92a‐1 augmented HBV replication. A computational analysis yielded potential binding sites for miR‐20a and miR‐92a‐1 in the HBV genome. The direct interaction between these two miRNAs and target regions in HBV transcripts was confirmed by luciferase reporter analysis. These results demonstrated negative feedback suppression of HBV replication by the miR‐17‐92 polycistron. J. Med. Virol. 85: 969–978, 2013. © 2013 Wiley Periodicals, Inc.