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Basic fibroblast growth factor induces proliferation of a rat pancreatic cancer cell line. Inhibition by somatostatin

✍ Scribed by M. Bensaïd; N. Tahiri-Jouti; C. Cambillau; N. Viguerie; B. Colas; C. Vidal; J. P. Tauber; J. P. Estève; C. Susini; N. Vaysse

Publisher
John Wiley and Sons
Year
1992
Tongue
French
Weight
466 KB
Volume
50
Category
Article
ISSN
0020-7136

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✦ Synopsis

AR4-2J, a rat pancreatic acinar-tumor cell line, was used to investigate long-term effects of basic fibroblast growth factor (bFGF) and somatostatin on pancreatic cancer cells. We observed that bFGF stimulated cell proliferation when cells were cultured in serum-free medium. The effect was dose-dependent with half-maximal and maximal effects at 25 pM and I nM bFGF, respectively. The somatostatin analog SMS 20 1-995 (SMS) decreased the growth-promoting effect of bFGF. The maximal effect was observed at I nM SMS and the half-maximal effect at 20 pM SMS. Characterization of bFGF receptor-binding properties with [i*Sl]bFGF revealed that AR4-2) cells exhibited 2 classes of bFGF binding site with respective K, values of 47 pM and 3 nM and binding capacities of I4 fmol and 0.9 pmol/ I O6 cells. High-affinity receptors correlated with bFGF stimulation of AR4-2J cell growth, suggesting that the effects of bFGF are receptor-mediated.

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