Hepatitis C virus NS2 protein activates cellular cyclic AMP-dependent pathways

Kyoung Mi Kim; Shi Nae Kwon; Ju Il Kang; Song Hee Lee; Sung Key Jang; Byung Yoon Ahn; Yoon Ki Kim

doi:10.1016/j.bbrc.2007.03.070

Hepatitis C virus NS2 protein activates cellular cyclic AMP-dependent pathways

Kyoung Mi Kim, Shi Nae Kwon, Ju Il Kang, Song Hee Lee, Sung Key Jang, Byung Yoon Ahn, Yoon Ki Kim

Research output: Contribution to journal › Article › peer-review

7 Citations (Scopus)

Abstract

Chronic infection of the hepatitis C virus (HCV) leads to liver cirrhosis and cancer. The mechanism leading to viral persistence and hepatocellular carcinoma, however, has not been fully understood. In this study, we show that the HCV infection activates cellular cAMP-dependent pathways. Expression of a luciferase reporter gene controlled by a basic promoter with the cAMP response element (CRE) was significantly elevated in human hepatoma Huh-7 cells infected with the HCV JFH1. Analysis with viral subgenomic replicons indicated that the HCV NS2 protein is responsible for the effect. Furthermore, the level of cellular transcripts whose stability is known to be regulated by cAMP was specifically reduced in cells harboring NS2-expressing replicons. These results allude to the HCV NS2 protein having a novel function of regulating cellular gene expression and proliferation through the cAMP-dependent pathway.

Original language	English
Pages (from-to)	948-954
Number of pages	7
Journal	Biochemical and biophysical research communications
Volume	356
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2007.03.070
Publication status	Published - 2007 May 18

Bibliographical note

Funding Information:
We are grateful to Dr. T. Wakita for providing us with pJFH1, Dr. R. Bartenschlager for HCV replicon constructs, and T.D. Kim, D.J. Jun, and K.T. Kim of Pohang University of Science and Technology for technical assistance. This work was supported in part by a grant (M103KB010020-06K0201-02020) of 21C Frontier Functional Human Genome Project from the Ministry of Science and Technology in Korea, the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MOST) (R01-2006-000-10194-0), and a Korea University Grant (K0518061).

Keywords

Cyclic AMP
Hepatitis C virus
Nonstructural protein 2
Transcription

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbrc.2007.03.070

Cite this

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title = "Hepatitis C virus NS2 protein activates cellular cyclic AMP-dependent pathways",

abstract = "Chronic infection of the hepatitis C virus (HCV) leads to liver cirrhosis and cancer. The mechanism leading to viral persistence and hepatocellular carcinoma, however, has not been fully understood. In this study, we show that the HCV infection activates cellular cAMP-dependent pathways. Expression of a luciferase reporter gene controlled by a basic promoter with the cAMP response element (CRE) was significantly elevated in human hepatoma Huh-7 cells infected with the HCV JFH1. Analysis with viral subgenomic replicons indicated that the HCV NS2 protein is responsible for the effect. Furthermore, the level of cellular transcripts whose stability is known to be regulated by cAMP was specifically reduced in cells harboring NS2-expressing replicons. These results allude to the HCV NS2 protein having a novel function of regulating cellular gene expression and proliferation through the cAMP-dependent pathway.",

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note = "Funding Information: We are grateful to Dr. T. Wakita for providing us with pJFH1, Dr. R. Bartenschlager for HCV replicon constructs, and T.D. Kim, D.J. Jun, and K.T. Kim of Pohang University of Science and Technology for technical assistance. This work was supported in part by a grant (M103KB010020-06K0201-02020) of 21C Frontier Functional Human Genome Project from the Ministry of Science and Technology in Korea, the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MOST) (R01-2006-000-10194-0), and a Korea University Grant (K0518061). ",

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AU - Ahn, Byung Yoon

AU - Kim, Yoon Ki

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N2 - Chronic infection of the hepatitis C virus (HCV) leads to liver cirrhosis and cancer. The mechanism leading to viral persistence and hepatocellular carcinoma, however, has not been fully understood. In this study, we show that the HCV infection activates cellular cAMP-dependent pathways. Expression of a luciferase reporter gene controlled by a basic promoter with the cAMP response element (CRE) was significantly elevated in human hepatoma Huh-7 cells infected with the HCV JFH1. Analysis with viral subgenomic replicons indicated that the HCV NS2 protein is responsible for the effect. Furthermore, the level of cellular transcripts whose stability is known to be regulated by cAMP was specifically reduced in cells harboring NS2-expressing replicons. These results allude to the HCV NS2 protein having a novel function of regulating cellular gene expression and proliferation through the cAMP-dependent pathway.

AB - Chronic infection of the hepatitis C virus (HCV) leads to liver cirrhosis and cancer. The mechanism leading to viral persistence and hepatocellular carcinoma, however, has not been fully understood. In this study, we show that the HCV infection activates cellular cAMP-dependent pathways. Expression of a luciferase reporter gene controlled by a basic promoter with the cAMP response element (CRE) was significantly elevated in human hepatoma Huh-7 cells infected with the HCV JFH1. Analysis with viral subgenomic replicons indicated that the HCV NS2 protein is responsible for the effect. Furthermore, the level of cellular transcripts whose stability is known to be regulated by cAMP was specifically reduced in cells harboring NS2-expressing replicons. These results allude to the HCV NS2 protein having a novel function of regulating cellular gene expression and proliferation through the cAMP-dependent pathway.

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Hepatitis C virus NS2 protein activates cellular cyclic AMP-dependent pathways

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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