BACKGROUND: Fibroblast growth factor-2 (FGF-2) has a role in the angiogenesis induced by renal carcinoma. MATERIALS AND METHODS: Blockage of FGF-2 by an antisense oligonucleotide (ASO) or by a mouse neutralizing anti-human FGF-2 monoclonal antibody (anti-FGF-2-mAb) was evaluated on a cell line isolated from a renal carcinoma bone metastasis (CRBM-1990), on Caki-1 and ACHN cells. Cocultures of endothelial cells and ASO- or mAb-treated carcinoma lines were investigated. RESULTS: Anti-FGF-2-mAb treatment induced a 33% reduction of FGF-2 released by ACHN, a 31% reduction of FGF-2 released by Caki-1, and a 70% reduction of FGF-2 released by CRBM-1990. ASO treatment did not inhibit endothelial cell proliferation. In contrast, anti-FGF-2-mAb significantly decreased endothelial cells proliferation induced by ACHN and CRBM-1990. The inhibition of endothelial cell growth was reverted by recombinant FGF-2. CONCLUSION: Modulation of FGF-2 production by renal cell carcinoma with a blocking mAb produced a significant inhibition of endothelial cell growth.
Inhibition of angiogenesis via FGF-2 blockage in primitive and bone metastatic renal cell carcinoma / Cenni E.; Perut F.; Granchi D.; Avnet S.; Amato I.; Brandi ML.; Giunti A.; Baldini N.. - In: ANTICANCER RESEARCH. - ISSN 0250-7005. - STAMPA. - 27(1A):(2007), pp. 315-319.
Inhibition of angiogenesis via FGF-2 blockage in primitive and bone metastatic renal cell carcinoma.
AVNET, SOFIA;GIUNTI, ARMANDO;BALDINI, NICOLA
2007
Abstract
BACKGROUND: Fibroblast growth factor-2 (FGF-2) has a role in the angiogenesis induced by renal carcinoma. MATERIALS AND METHODS: Blockage of FGF-2 by an antisense oligonucleotide (ASO) or by a mouse neutralizing anti-human FGF-2 monoclonal antibody (anti-FGF-2-mAb) was evaluated on a cell line isolated from a renal carcinoma bone metastasis (CRBM-1990), on Caki-1 and ACHN cells. Cocultures of endothelial cells and ASO- or mAb-treated carcinoma lines were investigated. RESULTS: Anti-FGF-2-mAb treatment induced a 33% reduction of FGF-2 released by ACHN, a 31% reduction of FGF-2 released by Caki-1, and a 70% reduction of FGF-2 released by CRBM-1990. ASO treatment did not inhibit endothelial cell proliferation. In contrast, anti-FGF-2-mAb significantly decreased endothelial cells proliferation induced by ACHN and CRBM-1990. The inhibition of endothelial cell growth was reverted by recombinant FGF-2. CONCLUSION: Modulation of FGF-2 production by renal cell carcinoma with a blocking mAb produced a significant inhibition of endothelial cell growth.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
