TY - JOUR
T1 - Inhibition of human breast epithelial HBL100 cell proliferation by a dextran derivative (CMDB7) with the FGF2 autocrine loop
AU - Bagheri-Yarmand, Rozita
AU - Liu, Jian Feng
AU - Ledoux, Dominique
AU - Morère, Jean François
AU - Crépin, Michel
N1 - Funding Information:
We thank Dr R.Vassy for his precious advice and Dr R. Hamlin and Pr J.P Caruelle and Dr T. Issad for critical review of the manuscript. This work was supported by `` Banque de la vie, Recherche Cancer'' and ``Fondation Martine Midy''.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1997/10/20
Y1 - 1997/10/20
N2 - Fibroblast growth factor 2 (FGF2) has been shown to be an autocrine growth factor in human breast epithelial cells HBL100. Here we studied the effects of one dextran derivative (CMDB7) on this autocrine loop. CMDB7 caused a dose-dependent decrease of HBL100 growth in serum-free medium. [3H]thymidine uptake in HBL100 cells and Balbc/3T3 cells by exogenous FGF2 was inhibited by CMDB7. Receptor binding assays with radio-iodinated FGF2, IGF1, EGF showed that CMDB7 only displaced the binding of 125I-FGF2 in a dose dependent manner. Scatchard analysis revealed that the presence of CMDB7 reduced 78% and 82% FGF2 binding capacity to its high and low affinity receptors respectively without altering the affinites of binding sites. These results suggest that CMDB7 exert its antiproliferative action on HBL100 cells by interfering with FGF2 autocrine loop.
AB - Fibroblast growth factor 2 (FGF2) has been shown to be an autocrine growth factor in human breast epithelial cells HBL100. Here we studied the effects of one dextran derivative (CMDB7) on this autocrine loop. CMDB7 caused a dose-dependent decrease of HBL100 growth in serum-free medium. [3H]thymidine uptake in HBL100 cells and Balbc/3T3 cells by exogenous FGF2 was inhibited by CMDB7. Receptor binding assays with radio-iodinated FGF2, IGF1, EGF showed that CMDB7 only displaced the binding of 125I-FGF2 in a dose dependent manner. Scatchard analysis revealed that the presence of CMDB7 reduced 78% and 82% FGF2 binding capacity to its high and low affinity receptors respectively without altering the affinites of binding sites. These results suggest that CMDB7 exert its antiproliferative action on HBL100 cells by interfering with FGF2 autocrine loop.
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U2 - 10.1006/bbrc.1997.7483
DO - 10.1006/bbrc.1997.7483
M3 - Article
C2 - 9344845
AN - SCOPUS:0031581052
SN - 0006-291X
VL - 239
SP - 424
EP - 428
JO - Biochemical and biophysical research communications
JF - Biochemical and biophysical research communications
IS - 2
ER -