Modulation of hepatitis B virus replication and hepatocyte differentiation by MicroRNA-1.

[Guest guest]

Hepatology. 2011 May;53(5):1476-85. doi: 10.1002/hep.24195.

Modulation of hepatitis B virus replication and hepatocyte differentiation by

MicroRNA-1.

Zhang X, Zhang E, Ma Z, Pei R, Jiang M, Schlaak JF, Roggendorf M, Lu M.

Source

Institute of Virology, University Hospital of Essen, Essen, Germany.

Abstract

MicroRNAs (miRNAs) are highly conserved small noncoding RNAs participating in

regulation of various cellular processes. Viruses have been shown to utilize

cellular miRNAs to increase their replication in host cells. Until now, the role

of miRNAs in hepatitis B virus (HBV) replication has remained largely unknown.

In this study, a number of miRNA mimics were transfected into hepatoma cell

lines with HBV replication. It was noted that microRNA-1 (miR-1) transfection

resulted in a marked increase of HBV replication, accompanied with up-regulated

HBV transcription, antigen expression, and progeny secretion. However,

bioinformatics and luciferase reporter analysis suggested that miR-1 may not

target the HBV genome directly but regulate the expression of host genes to

enhance HBV replication. Further studies showed that miR-1 was able to enhance

the HBV core promoter transcription activity by augmenting farnesoid X receptor

á expression. In addition, miR-1 arrested the cell cycle at the G(1) phase and

inhibited cell proliferation by targeting histone deacetylase 4 and E2F

transcription factor 5. Analysis of the cellular gene expression profile

indicated that miR-1 transfected hepatoma cells developed a differentiated

phenotype of hepatocytes. Conclusion: MiR-1 regulates the expression of several

host genes to enhance HBV replication and reverse cancer cell phenotype, which

is apparently beneficial for HBV replication. Our findings provide a novel

perspective on the role of miRNAs in host-virus interactions in HBV infection.

(HEPATOLOGY 2011;)

Copyright © 2011 American Association for the Study of Liver Diseases.

PMID: 21520166 [PubMed - in process]

[Guest guest]

Hepatology. 2011 May;53(5):1476-85. doi: 10.1002/hep.24195.

Modulation of hepatitis B virus replication and hepatocyte differentiation by

MicroRNA-1.

Zhang X, Zhang E, Ma Z, Pei R, Jiang M, Schlaak JF, Roggendorf M, Lu M.

Source

Institute of Virology, University Hospital of Essen, Essen, Germany.

Abstract

MicroRNAs (miRNAs) are highly conserved small noncoding RNAs participating in

regulation of various cellular processes. Viruses have been shown to utilize

cellular miRNAs to increase their replication in host cells. Until now, the role

of miRNAs in hepatitis B virus (HBV) replication has remained largely unknown.

In this study, a number of miRNA mimics were transfected into hepatoma cell

lines with HBV replication. It was noted that microRNA-1 (miR-1) transfection

resulted in a marked increase of HBV replication, accompanied with up-regulated

HBV transcription, antigen expression, and progeny secretion. However,

bioinformatics and luciferase reporter analysis suggested that miR-1 may not

target the HBV genome directly but regulate the expression of host genes to

enhance HBV replication. Further studies showed that miR-1 was able to enhance

the HBV core promoter transcription activity by augmenting farnesoid X receptor

á expression. In addition, miR-1 arrested the cell cycle at the G(1) phase and

inhibited cell proliferation by targeting histone deacetylase 4 and E2F

transcription factor 5. Analysis of the cellular gene expression profile

indicated that miR-1 transfected hepatoma cells developed a differentiated

phenotype of hepatocytes. Conclusion: MiR-1 regulates the expression of several

host genes to enhance HBV replication and reverse cancer cell phenotype, which

is apparently beneficial for HBV replication. Our findings provide a novel

perspective on the role of miRNAs in host-virus interactions in HBV infection.

(HEPATOLOGY 2011;)

Copyright © 2011 American Association for the Study of Liver Diseases.

PMID: 21520166 [PubMed - in process]