Overexpression of a DEAD box/RNA helicase protein, rck/p54, in human hepatocytes from patients with hepatitis C virus-related chronic hepatitis and its implication in hepatocellular carcinogenesis

K. Miyaji, Yoshihito Nakagawa, K. Matsumoto, H. Yoshida, H. Morikawa, Y. Hongou, Y. Arisaka, H. Kojima, T. Inoue, I. Hirata, K. Katsu, Yukihiro Akao

Research output: Contribution to journalArticle

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Abstract

Hepatitis C virus (HCV) infection is the most common cause of chronic hepatitis, which frequently progresses to hepatocellular carcinoma. The pathogenesis of its persistent infection and tumour progression has not been fully characterized yet. The RCK gene was previously cloned at the breakpoint of the t(11;14)(q23;q32) chromosome translocation observed in human B-cell lymphoma cell line RC-K8. The RCK protein, rck/p54, which is a 54-kDa cytoplasmic protein belonging to the DEAD box/RNA helicase family, is considered to facilitate the translation of mRNA(s) of genes for cell proliferation and malignant transformation not only in B-cell lymphomas having the t(11;14) translocation but also in other solid tumours. The aim of this work was to examine the involvement of rck/p54 in carcinogenesis of hepatocellular carcinoma from HCV-related chronic hepatitis. We examined the expression of rck/p54 in 29 cases of HCV-related chronic hepatitis and eight cases of hepatocellular carcinoma by immunohistochemistry and Western blot analysis. Twenty-six of 29 cases with HCV-related chronic hepatitis and all cases with hepatocellular carcinoma tested overexpressed rck/p54 protein. The expression of rck/p54 was lowered by treatment with IFN-α in two cases who showed the decrease in HCV RNA levels. These findings suggest that rck/p54 protein is possibly involved in the replication of HCV genomes in hepatocytes and in tumourigenesis of hepatocellular carcinomas.

Original languageEnglish
Pages (from-to)241-248
Number of pages8
JournalJournal of Viral Hepatitis
Volume10
Issue number4
DOIs
Publication statusPublished - 01-07-2003

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DEAD-box RNA Helicases
Chronic Hepatitis
Hepacivirus
Hepatocytes
Carcinogenesis
Hepatocellular Carcinoma
Proteins
B-Cell Lymphoma
Protein Biosynthesis
Virus Diseases
Genes
Neoplasms
Chromosomes
Western Blotting
Immunohistochemistry
Cell Proliferation
Genome
RNA
Cell Line
Infection

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Infectious Diseases
  • Virology

Cite this

Miyaji, K. ; Nakagawa, Yoshihito ; Matsumoto, K. ; Yoshida, H. ; Morikawa, H. ; Hongou, Y. ; Arisaka, Y. ; Kojima, H. ; Inoue, T. ; Hirata, I. ; Katsu, K. ; Akao, Yukihiro. / Overexpression of a DEAD box/RNA helicase protein, rck/p54, in human hepatocytes from patients with hepatitis C virus-related chronic hepatitis and its implication in hepatocellular carcinogenesis. In: Journal of Viral Hepatitis. 2003 ; Vol. 10, No. 4. pp. 241-248.
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Overexpression of a DEAD box/RNA helicase protein, rck/p54, in human hepatocytes from patients with hepatitis C virus-related chronic hepatitis and its implication in hepatocellular carcinogenesis. / Miyaji, K.; Nakagawa, Yoshihito; Matsumoto, K.; Yoshida, H.; Morikawa, H.; Hongou, Y.; Arisaka, Y.; Kojima, H.; Inoue, T.; Hirata, I.; Katsu, K.; Akao, Yukihiro.

In: Journal of Viral Hepatitis, Vol. 10, No. 4, 01.07.2003, p. 241-248.

Research output: Contribution to journalArticle

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AU - Miyaji, K.

AU - Nakagawa, Yoshihito

AU - Matsumoto, K.

AU - Yoshida, H.

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AU - Hongou, Y.

AU - Arisaka, Y.

AU - Kojima, H.

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AB - Hepatitis C virus (HCV) infection is the most common cause of chronic hepatitis, which frequently progresses to hepatocellular carcinoma. The pathogenesis of its persistent infection and tumour progression has not been fully characterized yet. The RCK gene was previously cloned at the breakpoint of the t(11;14)(q23;q32) chromosome translocation observed in human B-cell lymphoma cell line RC-K8. The RCK protein, rck/p54, which is a 54-kDa cytoplasmic protein belonging to the DEAD box/RNA helicase family, is considered to facilitate the translation of mRNA(s) of genes for cell proliferation and malignant transformation not only in B-cell lymphomas having the t(11;14) translocation but also in other solid tumours. The aim of this work was to examine the involvement of rck/p54 in carcinogenesis of hepatocellular carcinoma from HCV-related chronic hepatitis. We examined the expression of rck/p54 in 29 cases of HCV-related chronic hepatitis and eight cases of hepatocellular carcinoma by immunohistochemistry and Western blot analysis. Twenty-six of 29 cases with HCV-related chronic hepatitis and all cases with hepatocellular carcinoma tested overexpressed rck/p54 protein. The expression of rck/p54 was lowered by treatment with IFN-α in two cases who showed the decrease in HCV RNA levels. These findings suggest that rck/p54 protein is possibly involved in the replication of HCV genomes in hepatocytes and in tumourigenesis of hepatocellular carcinomas.

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