Factores de crecimiento y oncogenes en adenocarcinomas mamarios inducidos por acetato de medroxyprogesterona en ratones BALB/c / Growth hormones and oncogenes in mammary adenocarcinomas induced by medroxyprogesterone acetate in BALB/c mice
Medicina [B.Aires]
; 57(Supl.2): 70-74, Ago. 1997.
Article
em Es
| BINACIS
| ID: bin-7446
Biblioteca responsável:
BR1.1
ABSTRACT
We have studied the involvement of growth factors (GF), their receptors (GF-R) and oncogenes in modulating tumor growth in the medroxyprogesterone acetate (MPA)-induced mammary tumor model in BALB/c mice. We demonstrated the presence of both ligands of the insulin-like growth factor family (IGF-I, IGF-II) and the two types of receptors (IGF-RI, IGF-RII). MPA upregulated IGF-II mRNA and protein levels in hormone-dependent lines (MPA-D). The progression to a hormone-independent phenotype was accompanied by a high constitutive expression of IGF-II and by a significant decrease in IGF-IIR number. An antisense strategy used to evaluate the role of IGF in the MPA-induced growth of epithelial MPA-D cells showed that IGF mediate progestin-induced mammary tumor growth by autocrine/intracrine pathways. We also studied the role of heregulins (HRG), the recently identified ligands for the c-erbB3 and c-erbB4 oncogenes. HRG mRNA expression was restricted to tumors of ductal origin. MPA induced an in vivo up-regulation of HRG expression. Finally, we also found that MPA may be exerting its proliferative effect on MPA-D lines by inhibiting the expression of transforming growth factor beta 1, (TGF-beta 1) and the lack of expression of TGF-beta 1 in hormone-independent tumors may be related to the acquisition of autonomous growth.(Au)
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Coleções:
06-national
/
AR
Base de dados:
BINACIS
Assunto principal:
Oncogenes
/
Adenocarcinoma
/
Transformação Celular Neoplásica
/
Substâncias de Crescimento
/
Receptores de Fatores de Crescimento
/
Neoplasias Mamárias Experimentais
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
Es
Revista:
Medicina [B.Aires]
Ano de publicação:
1997
Tipo de documento:
Article