論文

査読有り
2004年10月

Overexpression of extracellular signal-regulated protein kinase and its correlation with proliferation in human hepatocellular carcinoma

LIVER INTERNATIONAL
  • Y Tsuboi
  • ,
  • T Ichida
  • ,
  • S Sugitani
  • ,
  • T Genda
  • ,
  • J Inayoshi
  • ,
  • M Takamura
  • ,
  • Y Matsuda
  • ,
  • M Nomoto
  • ,
  • Y Aoyagi

24
5
開始ページ
432
終了ページ
436
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1111/j.1478-3231.2004.0940.x
出版者・発行元
BLACKWELL MUNKSGAARD

Background: Dysregulation of cell proliferation is one of the most important features of human cancers including hepatocellular carcinoma (HCC). However, the molecular basis underlying the proliferation of HCC has not been fully clarified. Because a previous study reported that overexpression of extracellular signal-regulated protein kinase (ERK), which transduces extracellular growth stimuli to the nuclei, was frequently observed in several human cancers, this study was performed to analyze the expression of ERK in human HCC and its correlation with HCC proliferation. Methods: Twenty-four paired samples of primary HCCs and corresponding noncancerous liver tissues, and six samples of histologically normal liver tissue were obtained from surgically resected materials. The expression of ERK was examined by immunoblotting and immunohistochemical analysis. Proliferative activity of each HCC was examined by immunohistochemical demonstration of proliferative cell nuclear antigen (PCNA). Results: The ERK1 and ERK2 expression in HCCs was significantly higher than that in noncancerous liver tissues, and the ERK1 expression in noncancerous liver tissues from patients with HCC was higher than that in tissue from normal liver. Immunohistochemical examination revealed enhanced accumulation of ERK1 in the nuclei of HCC cells. Regression analysis revealed a significant correlation between ERK expression and PCNA labeling index in HCC. Conclusions: Our findings suggest that ERK overexpression contributes to the proliferation of HCC.

リンク情報
DOI
https://doi.org/10.1111/j.1478-3231.2004.0940.x
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/15482339
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000224433500007&DestApp=WOS_CPL
ID情報
  • DOI : 10.1111/j.1478-3231.2004.0940.x
  • ISSN : 1478-3223
  • PubMed ID : 15482339
  • Web of Science ID : WOS:000224433500007

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