Human interleukin 6 gene is activated by hepatitis B virus-X protein in human hepatoma cells

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dc.contributor.authorYoon Ik Lee-
dc.contributor.authorUi Sun Park-
dc.contributor.authorIn Pyo Choi-
dc.contributor.authorSeung Kew Yoon-
dc.contributor.authorYoung Min Park-
dc.contributor.authorYoung Ik Lee-
dc.date.accessioned2017-04-19T08:55:53Z-
dc.date.available2017-04-19T08:55:53Z-
dc.date.issued1998-
dc.identifier.issn1078-0432-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/4644-
dc.description.abstractInterleukin 6 (IL-6) is a pleiotropic cytokine that induces many biological activities, including some aspects of the immune reaction and inflammatory responses. In the liver, IL-6 regulates the synthesis of a broad spectrum of acute-phase proteins. IL-6 is also known to be a factor involved in the immunoregulatory perturbations in patients with chronic liver diseases (CLDs). Here, we report that IL-6 can be induced by hepatitis B virus (HBV)- X protein, as evidenced by high levels of serum IL-6 in patients with CLD with HBV infection, IL-6 productions observed in HBV-X-transfected cells, and transcriptional transactivations of the IL-6 gene by HBV-X. We determined serum levels of IL-6 in patients with chronic hepatitis B (CH-B), chronic hepatitis C (CH-C), liver cirrhosis (LC) caused by hepatitis B, and LC with hepatocellular carcinoma (HCC) caused by hepatitis B (LC+HCC). Mean serum levels of IL-6 in all CLD patients were higher than those in normal controls, and the difference was statistically significant (P < 0.05). Mean IL-6 levels of LC and LC+HCC patients were significantly higher than those of CH-B patients (P < 0.05). Because the etiological factor in all cases except CH-C (CH-B, LC, and LC+HCC) was HBV, we checked the possibility of HBV- transactivator-X activation of IL-6 promoter. Using deletion constructs of 5'-flanking regulatory regions of the IL-6 gene linked to the chloramphenicol acetyltransferase gene as a reporter, we found that the binding of nuclear factor-κB to a cis element is essential and sufficient for the induction of the IL-6 gene by HBV-X. We also found that HBV-X enhances the binding of two subunits of nuclear factor-κB (p65 and p52) to their target DNA binding sequences. These observations are relevant, in that HBV-X might play an important role in hepatic inflammation and diseases by up-regulating IL-6 production, which can eventually lead to LC and HCC.-
dc.publisherAmer Assoc Cancer Research-
dc.titleHuman interleukin 6 gene is activated by hepatitis B virus-X protein in human hepatoma cells-
dc.title.alternativeHuman interleukin 6 gene is activated by hepatitis B virus-X protein in human hepatoma cells-
dc.typeArticle-
dc.citation.titleClinical Cancer Research-
dc.citation.number7-
dc.citation.endPage1717-
dc.citation.startPage1711-
dc.citation.volume4-
dc.contributor.affiliatedAuthorYoon Ik Lee-
dc.contributor.affiliatedAuthorUi Sun Park-
dc.contributor.affiliatedAuthorIn Pyo Choi-
dc.contributor.affiliatedAuthorYoung Ik Lee-
dc.contributor.alternativeName이윤익-
dc.contributor.alternativeName박의선-
dc.contributor.alternativeName최인표-
dc.contributor.alternativeName윤승규-
dc.contributor.alternativeName박영민-
dc.contributor.alternativeName이영익-
dc.identifier.bibliographicCitationClinical Cancer Research, vol. 4, no. 7, pp. 1711-1717-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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