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Basic fibroblast growth factor induces proliferation of a rat pancreatic cancer cell line. Inhibition by somatostatin
Author(s) -
Bensaïd M.,
TahiriJouti N.,
Cambillau C.,
Viguerie N.,
Colas B.,
Vidal C.,
Tauber J. P.,
Estève J. P.,
Susini C.,
Vaysse N.
Publication year - 1992
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/ijc.2910500522
Subject(s) - basic fibroblast growth factor , somatostatin , endocrinology , medicine , stimulation , receptor , cell culture , growth factor , cell growth , biology , pancreatic cancer , fibroblast growth factor , fibroblast , cell , somatostatin receptor , somatostatin receptor 2 , cancer , biochemistry , genetics
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 201–995 (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 [ 125 I]bFGF revealed that AR4–2J cells exhibited 2 classes of bFGF binding site with respective K D values of 47 pM and 3 nM and binding capacities of 14 fmol and 0.9 pmol/10 6 cells. High‐affinity receptors correlated with bFGF stimulation of AR4–2J cell growth, suggesting that the effects of bFGF are receptor‐mediated.