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High expression of heparin‐binding EGF‐like growth factor in rat hepatocarcinogenesis
Author(s) -
Miyoshi Eiji,
Higashiyama Shigeki,
Nakagawa Takatoshi,
Suzuki Keiichiro,
Horimoto Masayoshi,
Hayashi Norio,
Fusamoto Hideyuki,
Kamada Takenobu,
Taniguchi Naoyuki
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19961009)68:2<215::aid-ijc13>3.0.co;2-9
Subject(s) - heparin binding egf like growth factor , epidermal growth factor , biology , cell culture , growth factor , messenger rna , endocrinology , medicine , microbiology and biotechnology , cancer research , gene , receptor , biochemistry , genetics
Heparin‐binding epidermal growth factor (EGF)‐like growth factor (HB‐EGF) is a member of the EGF family and is highly expressed in hepatoma tissues but not in normal liver. However, it is unknown when HB‐EGF is induced during hepatocarcinogenesis and what are the mechanisms underlying its high expression in hepatoma. To address this issue, the expression of HB‐EGF was investigated during hepatocarcinogenesis in LEC (Long‐Evans with a cinnamon‐like coat color) rats, which spontaneously develop hepatitis and hepatoma. LEA (Long‐Evans with an agouti coat color) rats were used as controls. Furthermore, the induction of HB‐EGF mRNA by various agents was investigated in a rat hepatoma cell line and hepatocytes in primary culture. Expression of HB‐EGF mRNA in the liver was very low at the stage of acute and chronic hepatitis and markedly increased at the stage of hepatoma in LEC rats. Non‐involved tissues adjacent to hepatoma showed low expression of HB‐EGF mRNA. Immunochemical studies revealed positive staining in hepatoma tissues. Induction of HB‐EGF mRNA by several growth factors was observed in a hepatoma cell line but not in normal hepatocytes. Our results suggest that HB‐EGF is associated with the early progression steps of hepatoma. © 1996 Wiley‐Liss, Inc.