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Titolo:
Inhibition of neuroblastoma-induced angiogenesis by fenretinide
Autore:
Ribatti, D; Alessandri, G; Baronio, M; Raffaghello, L; Cosimo, E; Marimpietri, D; Montaldo, PG; De Falco, G; Caruso, A; Vacca, A; Ponzoni, M;
Indirizzi:
Univ Bari, Policlin Bari, Dept Human Anat & Histol, I-70124 Bari, Italy Univ Bari Bari Italy I-70124 pt Human Anat & Histol, I-70124 Bari, Italy Univ Brescia, Inst Microbiol, Brescia, Italy Univ Brescia Brescia ItalyUniv Brescia, Inst Microbiol, Brescia, Italy G Gaslini Childrens Hosp, Lab Oncol, Genoa, Italy G Gaslini Childrens Hosp Genoa Italy rens Hosp, Lab Oncol, Genoa, Italy Univ Bari, Dept Biomed Sci & Human Oncol, Bari, Italy Univ Bari Bari Italy v Bari, Dept Biomed Sci & Human Oncol, Bari, Italy
Titolo Testata:
INTERNATIONAL JOURNAL OF CANCER
fascicolo: 3, volume: 94, anno: 2001,
pagine: 314 - 321
SICI:
0020-7136(20011101)94:3<314:IONABF>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIAL GROWTH-FACTOR; EMBRYO CHORIOALLANTOIC MEMBRANE; TUMOR PROGRESSION; FACTOR VEGF; IN-VIVO; CELLS; EXPRESSION; RETINOIDS; CANCER; DIFFERENTIATION;
Keywords:
angiogenesis; anti-angiogenesis; fenretinide; neuroblastoma;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Ribatti, D Univ Bari, Policlin Bari, Dept Human Anat & Histol, Piazza Giulio Cesare 11, I-70124 Bari, Italy Univ Bari Piazza Giulio Cesare 11 Bari Italy I-70124 ri, Italy
Citazione:
D. Ribatti et al., "Inhibition of neuroblastoma-induced angiogenesis by fenretinide", INT J CANC, 94(3), 2001, pp. 314-321

Abstract

Retinoids are a class of natural or synthetic compounds that participate in the control of cell proliferation, differentiation and fetal development. The synthetic retinoid fenretinide (HPR) inhibits carcinogenesis in various animal models. Retinoids have also been suggested to be effective inhibitors of angiogenesis. The effects of HPR on certain endothelial cell functions were investigated in vitro, and its effects on angiogenesis was studied in vivo, by using the chorioallantoic membrane (CAM) assay. HPR inhibited vascular endothelial growth factor- (VEGF-) and fibroblast growth factor-2- (FGF-2)-induced endothelial cell proliferation without affecting endothelial motility; moreover, HPR inhibited growth factor-induced angiogenesis in the CAM assay. Furthermore, a significant antiangiogenic potential of HPR has also been observed in neuroblastoma (NB) biopsy-induced angiogenesis in vivo. We previously demonstrated that supernatants derived from NB cell lines stimulated endothelial cell proliferation. In the present study, we foundthat this effect was abolished when NB cells were incubated in the presence of HPR. VEGF- and FGF-2-specific ELISA assays, performed on both NB cellsderived from conditioned medium and cellular extracts, indicated no consistent effect of HPR on the level of these angiogenic cytokines. Moreover, RT-PCR analysis of VEGF- and FGF-2 gene expression confirmed the above lack of effect. HPR was also able to significantly repress the spontaneous growthof endothelial cells, requiring at least 48-72 hr of treatment with HPR, followed by a progressive accumulation of cells in G, at subsequent time points. Finally, immunohistochemistry experiments performed in the CAM assay demonstrated that endothelial staining of both VEGF receptor 2 and FGF-2 receptor-2 was reduced after implantation of HPR-loaded sponges, as compared to control CAMs. These data suggest that HPR exerts its antiangiogenic activity through both a direct effect on endothelial cell proliferative activityand an inhibitory effect on the responsivity of the endothelial cells to the proliferative stimuli mediated by angiogenic growth factors. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 19:21:44