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Proteomic profiling of proteins decreased in hepatocellular carcinoma from patients infected with hepatitis C virus
Author(s) -
Yokoyama Yuichiro,
Kuramitsu Yasuhiro,
Takashima Motonari,
Iizuka Norio,
Toda Toshifusa,
Terai Shuji,
Sakaida Isao,
Oka Masaaki,
Nakamura Kazuyuki,
Okita Kiwamu
Publication year - 2004
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200300712
Subject(s) - hepatocellular carcinoma , aldolase a , peptide mass fingerprinting , hepatitis c virus , carcinogenesis , proteome , biology , microbiology and biotechnology , tropomyosin , transthyretin , hepatitis b virus , albumin , virus , proteomics , chemistry , cancer research , virology , enzyme , biochemistry , actin , cancer , genetics , endocrinology , gene
Hepatocellular carcinoma (HCC) is a major cause of death in Japan. It has been suggested that hepatitis C virus (HCV) plays an important role in hepatocarcinogenesis, because of high incidence among the patients. To understand the mechanism of hepatocarcinogenesis after HCV infection, we performed a comparative study on the protein profiles between tumorous and nontumorous specimens from the patients infected with HCV by means of two‐dimensional electrophoresis. Eleven spots were decreased in HCC tissues from over 50% of the patients. Eight proteins out of 11 spots were identified using peptide mass fingerprinting with matrix‐assisted laser desorption/ionization‐time of flight‐mass spectrometry. These proteins were liver type aldolase, tropomyosin β‐chain, ketohexokinase, enoyl‐CoA hydratase, albumin, smoothelin, ferritin light chain, and arginase 1. The intensity of enoyl‐CoA hydratase, tropomyosin β‐chain, ketohexokinase, liver type aldolase, and arginase 1 was significantly different ( p < 0.05). The decrease of 8 proteins was characteristic in HCC. We will discuss the implication of these proteins for the loss of function of hepatocytes and for the possibility of carcinogenesis of HCV‐related HCC.