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Expressions of basic fibroblast growth factor and its receptors and their relationship to proliferation of human hepatocellular carcinoma cell lines
Author(s) -
Ogasawara S,
Yano H,
Iemura A,
Hisaka T,
Kojiro M
Publication year - 1996
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510240132
Subject(s) - paracrine signalling , autocrine signalling , basic fibroblast growth factor , cell culture , cell growth , fibroblast growth factor receptor , biology , fibroblast growth factor , receptor , growth factor , cancer research , microbiology and biotechnology , endocrinology , medicine , biochemistry , genetics
On six human hepatocellular carcinoma (HCC) cell lines (KIM‐1, KYN‐1, KYN‐2, KYN‐3, HAK‐1A, and HAK‐1B), we examined expressions and functions of the proteins and messenger RNAs (mRNAs) of basic fibroblast growth factor (bFGF) and its receptor, i.e., fibroblast growth factor receptor‐1 (FGFR‐1), as well as mRNA expressions of FGFR‐2 approximately 4. All six cell lines expressed the proteins and mRNAs of bFGF and FGFR‐1, and at least one of FGFR‐2 approximately 4 mRNAs. Two of the six cell lines (KYN‐1 and KYN‐3) presented significant release of bFGF in culture supernatant, while the release in the remaining four cell lines was quite small. Addition of anti‐bFGF neutralizing antibody (1, 10, or 20 microg/mL) to culture medium resulted in marked suppression of cell proliferation in all cell lines except HAK‐1A. On the other hand, addition of exogenous bFGF (0.1, 1, or 5 ng/mL) to culture medium stimulated cell proliferation except in KIM‐1 and KYN‐2. When KIM‐1 was transplanted to nude mice and anti‐bFGF antibody was injected subcutaneously to a space surrounding the developed tumor, tumor proliferation was significantly suppressed in nude mice that received anti‐bFGF antibody than in control mice, but there were no histological differences between the groups, including blood space formation in the stroma. In conclusion, hepatocellular carcinoma (HCC) cells may possess a proliferation mechanism regulated by an autocrine mechanism, a paracrine mechanism, or both, which are mediated by bFGF/FGFR.