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Abstract:

The present study addresses the effect of targeting type I insulin-like growth factor receptor (IGF-IR) with antisense strategies in in vivo growth of breast cancer cells. Our research was carried out on C4HD tumors from an experimental model of hormonal carcinogenesis in which the synthetic progestin medroxyprogesterone acetate (MPA) induced mammary adenocarcinomas in Balb/c mice. We employed two different experimental strategies. With the first one we demonstrated that direct intratumor injection of phospliorothioate antisense oligodeoxynucleotides (AS[S]ODNs) to IGF-IR mRNA resulted in a significant inhibition of G4HD tumor growth. In the second experimental strategy, we assessed the effect of intravenous (i.v.) injection of AS [S]ODN on C4HD tumor growth. This systemic treatment also resulted in significant reduction in tumor growth. The antitumor effect of IGF-Il AS[S]ODNs in both experimental protocols was due to a specific antisense mechanism, since growth inhibition was dose-dependent and no abrogation of tumor proliferation was observed in mice treated with phosphorothioate sense ODNs (S[S]ODNs). In addition, IGF-IR expression was inhibited in tumors from mice receiving AS[S]ODNs, as compared to tumors from control groups. We then investigated signal transduction pathways modulated in vivo by AS[S]ODNs treatment. Tumors from AS[S]ODN-treated mice of both intratumoral and intravenous protocols showed a significant decrease in the degree of insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation. Activation of two of the main IGF-IR signaling pathways, phosphatidylinositol 3-kinase (PI-3K)/Akt and p42/p44 mitogen-activated protein kinases (IVIAPK) was abolished in tumors growing in AS[S]ODN-treated animals. Moreover, ErbB-2 tyrosine phosphorylation was blocked by in vivo administration of AS[S]ODNs. On the other hand, we found no regulation of either progesterone receptor expression or activity by in vivo AS[S]ODNs administration. Our results for the first time demonstrated that breast cancer growth can be inhibited by direct in vivo administration of IGF-IR AS[S]ODNs.

Registro:

Documento: Artículo
Título:Inhibition of in vivo breast cancer growth by antisense oligodeoxynucleptides to type I insulin-like growth factor receptor rnRNA involves inactivation of ErbBs, PI-3K/Akt and p42/p44 MAPK signaling pathways but not modulation of progesterone receptor activity
Autor:Salatino, M.; Schillaci, R.; Proietti, C.J.; Carnevale, R.; Frahm, I.; Molinolo, A.A.; Iribarren, A.; Charreau, E.H.; Elizalde, P.V.
Filiación:Lab. Molec. Mechanisms C., Inst. de Biol. Y Med. Experimental, CONICET, Obligado 2490, Buenos Aires 1428, Argentina
Servicio de Patología, Sanatoria Mater Dei, Buenos Aires, Argentina
Inst. Invest. Ing. Genet. Biol. M., Argentina
Palabras clave:Antisense strategies; Breast cancer; IGF-IR; antisense oligodeoxynucleotide; epidermal growth factor receptor; insulin receptor substrate 1; medroxyprogesterone acetate; messenger RNA; mitogen activated protein kinase; oligodeoxynucleotide phosphorothioate; phosphatidylinositol 3 kinase; progesterone receptor; protein p42; protein p44; somatomedin C receptor; tyrosine; antisense oligodeoxynucleotide; messenger RNA; mitogen activated protein kinase 1; phosphatidylinositol 3 kinase; progesterone receptor; somatomedin C receptor; animal cell; animal experiment; animal model; animal tissue; article; breast adenocarcinoma; breast cancer; cancer cell; cancer growth; cancer inhibition; carcinogenesis; cell proliferation; control group; controlled study; dose response; drug mechanism; experimental model; experimental mouse; female; in vivo study; mouse; nonhuman; priority journal; protein expression; protein phosphorylation; protein targeting; signal transduction; statistical significance; animal; Bagg albino mouse; cancer transplantation; cell culture; cell division; drug antagonism; drug effect; enzyme activation; epithelium cell; experimental neoplasm; genetics; metabolism; pathology; proto oncogene; Animalia; 1-Phosphatidylinositol 3-Kinase; Animals; Cell Division; Dose-Response Relationship, Drug; Enzyme Activation; Epithelial Cells; Female; Genes, erbB-1; Mammary Neoplasms, Experimental; Mice; Mice, Inbred BALB C; Mitogen-Activated Protein Kinase 1; Neoplasm Transplantation; Oligodeoxyribonucleotides, Antisense; Receptor, IGF Type 1; Receptors, Progesterone; RNA, Messenger; Signal Transduction; Tumor Cells, Cultured
Año:2004
Volumen:23
Número:30
Página de inicio:5161
Página de fin:5174
DOI: http://dx.doi.org/10.1038/sj.onc.1207659
Título revista:Oncogene
Título revista abreviado:Oncogene
ISSN:09509232
CODEN:ONCNE
CAS:insulin receptor substrate 1, 175335-32-7; medroxyprogesterone acetate, 71-58-9; mitogen activated protein kinase, 142243-02-5; phosphatidylinositol 3 kinase, 115926-52-8; tyrosine, 16870-43-2, 55520-40-6, 60-18-4; mitogen activated protein kinase 1, 137632-08-7; 1-Phosphatidylinositol 3-Kinase, EC 2.7.1.137; Mitogen-Activated Protein Kinase 1, EC 2.7.1.37; Oligodeoxyribonucleotides, Antisense; Receptor, IGF Type 1, EC 2.7.1.112; Receptors, Progesterone; RNA, Messenger
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09509232_v23_n30_p5161_Salatino

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Citas:

---------- APA ----------
Salatino, M., Schillaci, R., Proietti, C.J., Carnevale, R., Frahm, I., Molinolo, A.A., Iribarren, A.,..., Elizalde, P.V. (2004) . Inhibition of in vivo breast cancer growth by antisense oligodeoxynucleptides to type I insulin-like growth factor receptor rnRNA involves inactivation of ErbBs, PI-3K/Akt and p42/p44 MAPK signaling pathways but not modulation of progesterone receptor activity. Oncogene, 23(30), 5161-5174.
http://dx.doi.org/10.1038/sj.onc.1207659
---------- CHICAGO ----------
Salatino, M., Schillaci, R., Proietti, C.J., Carnevale, R., Frahm, I., Molinolo, A.A., et al. "Inhibition of in vivo breast cancer growth by antisense oligodeoxynucleptides to type I insulin-like growth factor receptor rnRNA involves inactivation of ErbBs, PI-3K/Akt and p42/p44 MAPK signaling pathways but not modulation of progesterone receptor activity" . Oncogene 23, no. 30 (2004) : 5161-5174.
http://dx.doi.org/10.1038/sj.onc.1207659
---------- MLA ----------
Salatino, M., Schillaci, R., Proietti, C.J., Carnevale, R., Frahm, I., Molinolo, A.A., et al. "Inhibition of in vivo breast cancer growth by antisense oligodeoxynucleptides to type I insulin-like growth factor receptor rnRNA involves inactivation of ErbBs, PI-3K/Akt and p42/p44 MAPK signaling pathways but not modulation of progesterone receptor activity" . Oncogene, vol. 23, no. 30, 2004, pp. 5161-5174.
http://dx.doi.org/10.1038/sj.onc.1207659
---------- VANCOUVER ----------
Salatino, M., Schillaci, R., Proietti, C.J., Carnevale, R., Frahm, I., Molinolo, A.A., et al. Inhibition of in vivo breast cancer growth by antisense oligodeoxynucleptides to type I insulin-like growth factor receptor rnRNA involves inactivation of ErbBs, PI-3K/Akt and p42/p44 MAPK signaling pathways but not modulation of progesterone receptor activity. Oncogene. 2004;23(30):5161-5174.
http://dx.doi.org/10.1038/sj.onc.1207659