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Characterization of tumors produced by signal peptide‐basic fibroblast growth factor‐transformed cells
Author(s) -
Rogelj Snezna,
Weinberg Robert A.,
Fanning Paul,
Klagsbrun Michael
Publication year - 1989
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240390103
Subject(s) - peptide , basic fibroblast growth factor , fibroblast growth factor receptor 3 , microbiology and biotechnology , fibroblast growth factor receptor , fibroblast growth factor receptor 4 , growth factor , chemistry , fibroblast growth factor , signal peptide , cancer research , biology , biochemistry , peptide sequence , receptor , gene
Basic fibroblast growth factor (bFGF) is found in a variety of cells and tissues. We have previously shown that bFGF is a transforming growth factor, but only when fused to a signal peptide (sp‐bFGF). Cells expressing the native bFGF are tumorigenic in nude mice only, where the tumors form at a low frequency and grow very slowly as compared to sp‐bFGF tumors. The cells transformed by the sp‐bFGF growth factor gene cause rapidly growing tumors within 10 days in 100% of syngeneic and nude mice. In nude mice, the tumors are highly vascularized, while the vascularization in immunocompetent syngeneic mice is not as prominent. The syngeneic mice have a characteristic humoral immune response to sp‐bFGF tumors, which differs from that mounted against ras ‐induced tumors. The ability of bFGF to induce tumorigenicity is significant in view of the recent discoveries of three new oncogenes: hst, int‐2 , and an oncogene from a human colon cancer. In addition to homology with FGF, the proteins encoded by these oncogenes all have a potential signal peptide at the protein's amino terminus, suggesting a mode of action analogous to that of our artificial signal peptide‐bFGF (sp‐bFGF) transforming growth factor model system.