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Expression of basic fibroblast growth factor and its receptor in an invasive bladder carcinoma cell line
Author(s) -
Allen Lynn E.,
Maher Pamela A.
Publication year - 1993
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041550218
Subject(s) - basic fibroblast growth factor , autocrine signalling , receptor , fibroblast growth factor , biology , paracrine signalling , fibroblast growth factor receptor 1 , angiogenesis , cell culture , cancer research , fibroblast growth factor receptor , microbiology and biotechnology , growth factor receptor inhibitor , growth factor , fibroblast growth factor receptor 2 , biochemistry , genetics
Basic fibroblast growth factor (bFGF) is a multifunctional growth factor that can stimulate cell proliferation, production of proteases, and angiogenesis. Loss of mechanisms that regulate bFGF activity could result in tumor development. To test this idea, cells derived from an invasive bladder carcinoma (EJ) were compared with cells derived from a noninvasive bladder carcinoma (RT4) for the expression of bFGF and high and low affinity FGF receptors. bFGF was produced by the invasive EJ cells but not by the noninvasive RT4 cells, suggesting that bFGF could act in an autocrine fashion in the EJ cells to promote their invasion and growth in the surrounding tissue. The two cells lines also showed differences in FGF receptor expression. The EJ cells expressed both high and low affinity FGF receptors as determined by Scatchard analysis, whereas the RT4 cells expressed only high affinity receptors. The high affinity receptors on the RT4 cells expressed recognized by an antibody to known FGF receptors. Furthermore, in contrast to the EJ cells, bFGF did not induce protein tyrosine phosphorylation in the RT4 cells. Thus these data suggest that the invasive potential of bladder carcinoma cells may be regulated by the expression of both bFGF and its receptors. © 1993 Wiley‐Liss, Inc.
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