Involvement of insulin-like growth factors-I and-II and their receptors in medroxyprogesterone acetate-induced growth of mouse mammary adenocarcinomas

The role of the insulin-like growth factors (IGFs) system was investigated in hormone-dependent (HD) and -independent (HI) in vivo lines of the medroxyprogesterone acetate (MPA)-induced mammary tumor model in Balb/c mice. IGF-II protein and message showed a three- to four-fold increase in HD lines g...

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Autor principal: Elizalde, P.V
Otros Autores: Lanari, C., Molinolo, A.A, Guerra, F.K, Balañá, M.E, Simian, M., Iribarren, A.M, Charreau, E.H
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 1998
Acceso en línea:Registro en Scopus
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024 7 |2 scopus  |a 2-s2.0-0032213229 
024 7 |2 cas  |a Insulin-Like Growth Factor I, 67763-96-6; Insulin-Like Growth Factor II, 67763-97-7; Medroxyprogesterone 17-Acetate, 71-58-9; Oligonucleotides, Antisense; Receptor, IGF Type 1, EC 2.7.1.112; Receptor, IGF Type 2 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a JSBBE 
100 1 |a Elizalde, P.V. 
245 1 0 |a Involvement of insulin-like growth factors-I and-II and their receptors in medroxyprogesterone acetate-induced growth of mouse mammary adenocarcinomas 
260 |c 1998 
270 1 0 |m Elizalde, P.V.; Instituto de Biologia/Medicina Exp., Obligado 2490, Buenos Aires 1428, Argentina; email: elizalde@proteus.dna.uba.ar 
506 |2 openaire  |e Política editorial 
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504 |a Beukers, M.W., Youngman, O., Zhang, H., Ling, N., Rosenfeld, R., (Leu 27) Insulin-like growth factor II is highly selective for the type-II IGF receptor in binding, cross-linking and thymidine incorporation experiments (1991) Endocrinology, 1128, pp. 1201-1203 
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520 3 |a The role of the insulin-like growth factors (IGFs) system was investigated in hormone-dependent (HD) and -independent (HI) in vivo lines of the medroxyprogesterone acetate (MPA)-induced mammary tumor model in Balb/c mice. IGF-II protein and message showed a three- to four-fold increase in HD lines growing in MPA-treated mice, as compared with HD tumors growing in untreated mice. Progression to a hormone-independent phenotype in all these lines was accompanied by a high constitutive expression of IGF-II. Similar IGF-I mRNA levels were detected in HD and HI lines. Both IGE-I and -II messages arose from the malignant epithelial cells, as shown by in situ hybridization studies. A significant decrease in Man-6P/type II IGF-R content was detected in HD tumors growing in MPA-treated mice as compared with HD lines growing in untreated mice. On the other hand, in HI tumors, notwithstanding high IGF-II synthesis, the levels of Man-6P/type II IGF-R remain high. Competitive inhibition and affinity labeling studies showed an almost exclusive binding of IGF-II to Man-6P/type II IGF-R on tumor membranes. The involvement of IGFs in the growth of epithelial primary cultures of the C4-HD line was evaluated. Exogenous IGF-I potentiated MPA stimulatory effect at concentrations of 50-100 ng/ml. Treatment of C4-HD cells with antisense oligodeoxynucleotides (ASODNs) to type I IGF-R and to IGF-II RNA resulted in a dose-dependent inhibition of MPA-mediated cell proliferation. The inhibition caused by IGF-II ASODNs could not be overcome by the addition of IGF-II up to 150 ng/ml. ASODNs to type I IGF-R at 40 μg/ml reduced by 75% the number of type I IGF-R; ASODNs to IGF-II at 1 μM decreased by 83% the levels of IGF-II protein. Our results provide support for the involvement of IGE-I and -II in MPA-induced mammary tumor growth by autocrine pathways.  |l eng 
536 |a Detalles de la financiación: National Council for Scientific Research 
536 |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas 
536 |a Detalles de la financiación: 94/120 N CRP/ARG 93-01 
536 |a Detalles de la financiación: Acknowledgements--The authors thank Dr A. R. Kornblihtt for useful advice and Dr E. Bal de Kier Joff6 for critical discussion and review of the manuscript. This work was supported by grants from The United Nations Industrial Development Organization, UNIDO Contract 94/120 N CRP/ARG 93-01, from the National Scientific Council of Argentina, CONICET, and from Fundacion SALES. 
593 |a Inst. de Biologia y Med. Exp. IBYME, Obligado 2490, Buenos Aires 1428, Argentina 
593 |a Inst. de Invest. en Ingeniera G., Obligado 2490, Buenos Aires 1428, Argentina 
690 1 0 |a SOMATOMEDIN B 
690 1 0 |a SOMATOMEDIN B RECEPTOR 
690 1 0 |a SOMATOMEDIN C 
690 1 0 |a SOMATOMEDIN C RECEPTOR 
690 1 0 |a ANIMAL CELL 
690 1 0 |a ANIMAL EXPERIMENT 
690 1 0 |a ANIMAL MODEL 
690 1 0 |a ANIMAL TISSUE 
690 1 0 |a ARTICLE 
690 1 0 |a BREAST ADENOCARCINOMA 
690 1 0 |a BREAST EPITHELIUM 
690 1 0 |a CANCER GROWTH 
690 1 0 |a CELL PROLIFERATION 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a FEMALE 
690 1 0 |a IN SITU HYBRIDIZATION 
690 1 0 |a MOUSE 
690 1 0 |a NONHUMAN 
690 1 0 |a PROTEIN EXPRESSION 
690 1 0 |a ADENOCARCINOMA 
690 1 0 |a ANIMALS 
690 1 0 |a BASE SEQUENCE 
690 1 0 |a CELL DIVISION 
690 1 0 |a FEMALE 
690 1 0 |a IN SITU HYBRIDIZATION 
690 1 0 |a INSULIN-LIKE GROWTH FACTOR I 
690 1 0 |a INSULIN-LIKE GROWTH FACTOR II 
690 1 0 |a MAMMARY NEOPLASMS, EXPERIMENTAL 
690 1 0 |a MEDROXYPROGESTERONE 17-ACETATE 
690 1 0 |a MICE 
690 1 0 |a MICE, INBRED BALB C 
690 1 0 |a OLIGONUCLEOTIDES, ANTISENSE 
690 1 0 |a RECEPTOR, IGF TYPE 1 
690 1 0 |a RECEPTOR, IGF TYPE 2 
690 1 0 |a TUMOR CELLS, CULTURED 
690 1 0 |a ANIMALIA 
700 1 |a Lanari, C. 
700 1 |a Molinolo, A.A. 
700 1 |a Guerra, F.K. 
700 1 |a Balañá, M.E. 
700 1 |a Simian, M. 
700 1 |a Iribarren, A.M. 
700 1 |a Charreau, E.H. 
773 0 |d 1998  |g v. 67  |h pp. 305-317  |k n. 4  |p J. Steroid Biochem. Mol. Biol.  |x 09600760  |w (AR-BaUEN)CENRE-5799  |t Journal of Steroid Biochemistry and Molecular Biology 
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856 4 0 |u https://hdl.handle.net/20.500.12110/paper_09600760_v67_n4_p305_Elizalde  |y Handle 
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