ID | 54186 |
JaLCDOI | |
フルテキストURL | |
著者 |
Sejima, Hiroe
Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Satoh, Shinya
Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Dansako, Hiromichi
Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Honda, Masao
Department of Gastroenterology, Kanazawa University Graduate School of Medicine
Kaneko, Shuichi
Department of Gastroenterology, Kanazawa University Graduate School of Medicine
Ikeda, Masanori
Department of Persistent and Oncogenic Viruses, Kagoshima University Graduate School of Medical and Dental Sciences
Kato, Nobuyuki
Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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抄録 | The mechanisms of hepatitis C virus (HCV)-associated hepatocarcinogenesis and disease progression are unclear. We previously observed that the expression level of carboxypeptidase B2 (CPB2) gene was remarkably suppressed by persistent HCV RNA replication in human hepatoma cell line Li23-derived cells. The results of the present study demonstrated that the CPB2 expression in patients with chronic hepatitis C was inversely correlated with several risk factors of hepatic fibrosis or steatosis, although ectopic CPB2 expression did not suppress the expression of fibrogenic or lipogenic genes. The suppressed CPB2 expression was restored by treatment with 5-azacytidine. To clarify the mechanism underlying this phenomenon, we analyzed the CPB2 promoter, and the results revealed that (1) hepatocyte nuclear factor 1 (HNF1), especially HNF1α, was essential for the CPB2 promoter, and (2) CPB2 promoter was not methylated by persistent HCV RNA replication. The expression levels of HNF1α and HNF1β were also not changed by persistent HCV RNA replication. These results suggest the existence of 5-azacytidine-inducible or -reducible unknown factor(s) that can control the CPB2 expression. To evaluate this idea we performed a microarray analysis, and several gene candidates corresponding to the suggested factor(s) were identified.
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キーワード | persistent hepatitis C virus replication
carboxypeptidase B2
suppression mechanism of CPB2 expression
DNA methylation
hepatocyte nuclear factor 1
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Amo Type | Original Article
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出版物タイトル |
Acta Medica Okayama
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発行日 | 2016-04
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巻 | 70巻
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号 | 2号
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出版者 | Okayama University Medical School
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開始ページ | 75
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終了ページ | 88
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ISSN | 0386-300X
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NCID | AA00508441
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資料タイプ |
学術雑誌論文
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言語 |
英語
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著作権者 | CopyrightⒸ 2016 by Okayama University Medical School
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論文のバージョン | publisher
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査読 |
有り
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PubMed ID | |
Web of Science KeyUT |