Type I insulin-like growth factor receptor antisense strategies in experimental breast cancer
We addressed the effect of targeting type I insulin-like growth factor receptor (IGF-IR), with antisense strategies in vivo growth of breast cancer cells. We used C4HD tumors from an experimental model of hormonal carcinogenesis in which medroxyprogesterone acetate induced mammary adenocarcinomas in...
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2004
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Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00257680_v64_n2_p129_Salatino http://hdl.handle.net/20.500.12110/paper_00257680_v64_n2_p129_Salatino |
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paper:paper_00257680_v64_n2_p129_Salatino2023-06-08T14:53:34Z Type I insulin-like growth factor receptor antisense strategies in experimental breast cancer Antisense strategies Breast cancer IGF-IR antisense oligodeoxynucleotide epidermal growth factor receptor 2 insulin receptor substrate 1 medroxyprogesterone acetate messenger RNA mitogen activated protein kinase oligodeoxynucleotide phosphorothioate progesterone receptor protein kinase B somatomedin C receptor animal cell animal experiment animal model article breast adenocarcinoma breast cancer cancer cell cancer growth cancer inhibition dose response drug targeting enzyme activation hormonal carcinogenesis in vivo culture mouse nonhuman protein expression protein phosphorylation protein targeting Adenocarcinoma Animal Diseases Animals Dose-Response Relationship, Drug Female Mammary Neoplasms, Experimental Medroxyprogesterone Mice Mice, Inbred BALB C Oligodeoxyribonucleotides, Antisense Receptor, IGF Type 1 Receptors, Somatomedin RNA, Messenger Tumor Cells, Cultured We addressed the effect of targeting type I insulin-like growth factor receptor (IGF-IR), with antisense strategies in vivo growth of breast cancer cells. We used C4HD tumors from an experimental model of hormonal carcinogenesis in which medroxyprogesterone acetate induced mammary adenocarcinomas in Balb/c mice. Intratumor or systemic administration of phosphorothiolated antisense oligodeoxynucleotides (AS[S]ODN) to IGF-IR mRNA resulted in a significant inhibition of C4HD tumor growth. The antitumor effect was specific since inhibition of tumor growth was dose-dependent and no effect was observed in mice treated with sense S[S]ODN. Tumors from AS[S]ODN-treated mice showed a decrease in IGF-IR expression and in insulin receptor substrate-1 tyrosine phosphorylation. Activation of PI-3K/Akt, p42/p44 MAPK and ErbB-2 was abolished in tumors treated with AS[S]ODN. Progesterone receptor expression or activity remained invariable. This is the first demonstration that breast cancer growth can be inhibited by direct in vivo administration of IGF-IR AS[S]ODN. 2004 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00257680_v64_n2_p129_Salatino http://hdl.handle.net/20.500.12110/paper_00257680_v64_n2_p129_Salatino |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
topic |
Antisense strategies Breast cancer IGF-IR antisense oligodeoxynucleotide epidermal growth factor receptor 2 insulin receptor substrate 1 medroxyprogesterone acetate messenger RNA mitogen activated protein kinase oligodeoxynucleotide phosphorothioate progesterone receptor protein kinase B somatomedin C receptor animal cell animal experiment animal model article breast adenocarcinoma breast cancer cancer cell cancer growth cancer inhibition dose response drug targeting enzyme activation hormonal carcinogenesis in vivo culture mouse nonhuman protein expression protein phosphorylation protein targeting Adenocarcinoma Animal Diseases Animals Dose-Response Relationship, Drug Female Mammary Neoplasms, Experimental Medroxyprogesterone Mice Mice, Inbred BALB C Oligodeoxyribonucleotides, Antisense Receptor, IGF Type 1 Receptors, Somatomedin RNA, Messenger Tumor Cells, Cultured |
spellingShingle |
Antisense strategies Breast cancer IGF-IR antisense oligodeoxynucleotide epidermal growth factor receptor 2 insulin receptor substrate 1 medroxyprogesterone acetate messenger RNA mitogen activated protein kinase oligodeoxynucleotide phosphorothioate progesterone receptor protein kinase B somatomedin C receptor animal cell animal experiment animal model article breast adenocarcinoma breast cancer cancer cell cancer growth cancer inhibition dose response drug targeting enzyme activation hormonal carcinogenesis in vivo culture mouse nonhuman protein expression protein phosphorylation protein targeting Adenocarcinoma Animal Diseases Animals Dose-Response Relationship, Drug Female Mammary Neoplasms, Experimental Medroxyprogesterone Mice Mice, Inbred BALB C Oligodeoxyribonucleotides, Antisense Receptor, IGF Type 1 Receptors, Somatomedin RNA, Messenger Tumor Cells, Cultured Type I insulin-like growth factor receptor antisense strategies in experimental breast cancer |
topic_facet |
Antisense strategies Breast cancer IGF-IR antisense oligodeoxynucleotide epidermal growth factor receptor 2 insulin receptor substrate 1 medroxyprogesterone acetate messenger RNA mitogen activated protein kinase oligodeoxynucleotide phosphorothioate progesterone receptor protein kinase B somatomedin C receptor animal cell animal experiment animal model article breast adenocarcinoma breast cancer cancer cell cancer growth cancer inhibition dose response drug targeting enzyme activation hormonal carcinogenesis in vivo culture mouse nonhuman protein expression protein phosphorylation protein targeting Adenocarcinoma Animal Diseases Animals Dose-Response Relationship, Drug Female Mammary Neoplasms, Experimental Medroxyprogesterone Mice Mice, Inbred BALB C Oligodeoxyribonucleotides, Antisense Receptor, IGF Type 1 Receptors, Somatomedin RNA, Messenger Tumor Cells, Cultured |
description |
We addressed the effect of targeting type I insulin-like growth factor receptor (IGF-IR), with antisense strategies in vivo growth of breast cancer cells. We used C4HD tumors from an experimental model of hormonal carcinogenesis in which medroxyprogesterone acetate induced mammary adenocarcinomas in Balb/c mice. Intratumor or systemic administration of phosphorothiolated antisense oligodeoxynucleotides (AS[S]ODN) to IGF-IR mRNA resulted in a significant inhibition of C4HD tumor growth. The antitumor effect was specific since inhibition of tumor growth was dose-dependent and no effect was observed in mice treated with sense S[S]ODN. Tumors from AS[S]ODN-treated mice showed a decrease in IGF-IR expression and in insulin receptor substrate-1 tyrosine phosphorylation. Activation of PI-3K/Akt, p42/p44 MAPK and ErbB-2 was abolished in tumors treated with AS[S]ODN. Progesterone receptor expression or activity remained invariable. This is the first demonstration that breast cancer growth can be inhibited by direct in vivo administration of IGF-IR AS[S]ODN. |
title |
Type I insulin-like growth factor receptor antisense strategies in experimental breast cancer |
title_short |
Type I insulin-like growth factor receptor antisense strategies in experimental breast cancer |
title_full |
Type I insulin-like growth factor receptor antisense strategies in experimental breast cancer |
title_fullStr |
Type I insulin-like growth factor receptor antisense strategies in experimental breast cancer |
title_full_unstemmed |
Type I insulin-like growth factor receptor antisense strategies in experimental breast cancer |
title_sort |
type i insulin-like growth factor receptor antisense strategies in experimental breast cancer |
publishDate |
2004 |
url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00257680_v64_n2_p129_Salatino http://hdl.handle.net/20.500.12110/paper_00257680_v64_n2_p129_Salatino |
_version_ |
1768542399691227136 |