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Titolo:
ENHANCEMENT OF TUMOR-GROWTH AND VASCULAR DENSITY BY TRANSFECTION OF VASCULAR ENDOTHELIAL-CELL GROWTH-FACTOR INTO MCF-7 HUMAN BREAST-CARCINOMA CELLS
Autore:
ZHANG HT; CRAFT P; SCOTT PAE; ZICHE M; WEICH HA; HARRIS AL; BICKNELL R;
Indirizzi:
UNIV OXFORD,JOHN RADCLIFFE HOSP,INST MOLEC MED,IMPERIAL CANC RES FUND,MOLEC ANGIOGENESIS GRP OXFORD OX3 9DU ENGLAND UNIV OXFORD,JOHN RADCLIFFE HOSP,INST MOLEC MED,IMPERIAL CANC RES FUND,MOLEC ANGIOGENESIS GRP OXFORD OX3 9DU ENGLAND
Titolo Testata:
Journal of the National Cancer Institute
fascicolo: 3, volume: 87, anno: 1995,
pagine: 213 - 219
Fonte:
ISI
Lingua:
ENG
Soggetto:
PERMEABILITY FACTOR; FACTOR FAMILY; CANCER-CELLS; FACTOR GENE; FACTOR-IV; ANGIOGENESIS; INVIVO; EXPRESSION; INHIBITION; INDICATOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
33
Recensione:
Indirizzi per estratti:
Citazione:
H.T. Zhang et al., "ENHANCEMENT OF TUMOR-GROWTH AND VASCULAR DENSITY BY TRANSFECTION OF VASCULAR ENDOTHELIAL-CELL GROWTH-FACTOR INTO MCF-7 HUMAN BREAST-CARCINOMA CELLS", Journal of the National Cancer Institute, 87(3), 1995, pp. 213-219

Abstract

Background: Vascular endothelial growth factor (VEGF) is a secreted endothelial-specific growth factor that is angiogenic in vivo, It is commonly expressed in a range of carcinomas, Purpose: The study was designed to investigate the effect of constitutive expression of VEGF on tumor formation by estrogen-dependent human MCF-7 breast carcinoma cells. Methods: A full-length complementary DNA encoding the shortest isoform of VEGF (VEGF(121)) was stably transfected into MCF-7 cells. Transfected clones were screened for VEGF(121) messenger RNA (mRNA) expression by ribonuclease protection analysis and for secretion of VEGF(121)protein by Western blot analysis. Secretion of biologically active VEGF(121) by transfectants was confirmed by 1) a competitive radioreceptor-binding assay, 2) stimulation of the growth of microvascular endothelial cells in vitro, and 3) potent angiogenic activity in the rabbit corneal assay, Tumor models were then established by subcutaneously implanting wildtype or VEGF(121)-transfected MCF-7 cells, together with either mouse BALB/3T3 clone A31 fibroblasts or human MDA-435S breast carcinoma cells, into ovariectomized nude mice either with or without aseparately implanted slow-release estrogen pellet. Tumor vascularity was quantitatively assessed by capillary vessel counting after staining with the pan-endothelial marker CD31. Results: Stable VEGF(121)-overexpressing MCF-7 cells were isolated and designated V12 cells. When implanted into the rabbit cornea, V12 cells elicited a strong directional outgrowth of capillaries. The growth rate of V12 cells in vitro was indistinguishable from that of MCF-7 wild-type cells, V12 cells formedfaster growing tumors than did wild-type cells (P<.01) when xenografted subcutaneously into nude mice with either 3T3 fibroblasts or MDA-435S cells, Tumors formed from V12 cells were more vascular (P<.01) and showed a heterogeneous distribution of vessels when compared with the homogeneous distribution seen in tumors formed from wild-type cells. VEGF(121) overexpression had no effect on hormone dependence or tamoxifen sensitivity of tumor formation by MCF-7 cells in mice, No macroscopic evidence for metastasis from subcutaneous implants was obtained, Conclusions: VEGF(121) expression by breast carcinoma cells confers a growth advantage in vivo but not in vitro, Tumors formed by V12 transfectants were more vascular than those formed by wild-type MCF-7 cells, and we surmise that the growth advantage arises from increased tumor vascularization induced by VEGF(121). Implications: Tumor formation by V12 cells could provide a useful model for the assessment of anti-angiogenic drugs.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 06:12:26