Activation of Stat3 by heregulin/ErbB-2 through the co-option of progesterone receptor signaling drives breast cancer growth

Cross talk between the steroid hormone receptors for estrogen and progesterone (PR) and the ErbB family of receptor tyrosine kinases appears to be a hallmark of breast cancer growth, but its underlying mechanism remains poorly explored. Here we have highlighted signal transducer and activator of tra...

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Autores principales: Proietti, C.J., Rosemblit, C., Beguelin, W., Rivas, M.A., Flaqué, M.C.D., Charreau, E.H., Schillaci, R., Elizalde, P.V.
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Acceso en línea:http://hdl.handle.net/20.500.12110/paper_02707306_v29_n5_p1249_Proietti
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spelling todo:paper_02707306_v29_n5_p1249_Proietti2023-10-03T15:14:50Z Activation of Stat3 by heregulin/ErbB-2 through the co-option of progesterone receptor signaling drives breast cancer growth Proietti, C.J. Rosemblit, C. Beguelin, W. Rivas, M.A. Flaqué, M.C.D. Charreau, E.H. Schillaci, R. Elizalde, P.V. epidermal growth factor receptor 2 estrogen receptor neu differentiation factor progesterone receptor STAT3 protein epidermal growth factor receptor 2 neu differentiation factor progesterone receptor STAT3 protein animal cell animal cell culture animal experiment animal model article Bagg albino mouse breast cancer cancer growth enzyme activity female immunoprecipitation mouse nonhuman priority journal signal transduction Western blotting animal cell proliferation experimental neoplasm metabolism pathology Animals Cell Proliferation Female Mammary Neoplasms, Animal Mice Mice, Inbred BALB C Neuregulin-1 Receptor, erbB-2 Receptors, Progesterone Signal Transduction STAT3 Transcription Factor Cross talk between the steroid hormone receptors for estrogen and progesterone (PR) and the ErbB family of receptor tyrosine kinases appears to be a hallmark of breast cancer growth, but its underlying mechanism remains poorly explored. Here we have highlighted signal transducer and activator of transcription 3 (Stat3) as a key protein activated by heregulin (HRG), a ligand of the ErbB receptors, through co-opted, ligand-independent PR function as a signaling molecule. Stat3 activation was an absolute requirement in HRG-induced mammary tumor growth, and targeting Stat3 effectively inhibited growth of breast cancer cells with activated HRG/ErbB-2 and PR. Our findings unravel a novel potential therapeutic intervention in PR- and ErbB-2-positive breast tumors, involving the specific blockage of PR signaling activity. Copyright © 2009, American Society for Microbiology. All Rights Reserved. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_02707306_v29_n5_p1249_Proietti
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic epidermal growth factor receptor 2
estrogen receptor
neu differentiation factor
progesterone receptor
STAT3 protein
epidermal growth factor receptor 2
neu differentiation factor
progesterone receptor
STAT3 protein
animal cell
animal cell culture
animal experiment
animal model
article
Bagg albino mouse
breast cancer
cancer growth
enzyme activity
female
immunoprecipitation
mouse
nonhuman
priority journal
signal transduction
Western blotting
animal
cell proliferation
experimental neoplasm
metabolism
pathology
Animals
Cell Proliferation
Female
Mammary Neoplasms, Animal
Mice
Mice, Inbred BALB C
Neuregulin-1
Receptor, erbB-2
Receptors, Progesterone
Signal Transduction
STAT3 Transcription Factor
spellingShingle epidermal growth factor receptor 2
estrogen receptor
neu differentiation factor
progesterone receptor
STAT3 protein
epidermal growth factor receptor 2
neu differentiation factor
progesterone receptor
STAT3 protein
animal cell
animal cell culture
animal experiment
animal model
article
Bagg albino mouse
breast cancer
cancer growth
enzyme activity
female
immunoprecipitation
mouse
nonhuman
priority journal
signal transduction
Western blotting
animal
cell proliferation
experimental neoplasm
metabolism
pathology
Animals
Cell Proliferation
Female
Mammary Neoplasms, Animal
Mice
Mice, Inbred BALB C
Neuregulin-1
Receptor, erbB-2
Receptors, Progesterone
Signal Transduction
STAT3 Transcription Factor
Proietti, C.J.
Rosemblit, C.
Beguelin, W.
Rivas, M.A.
Flaqué, M.C.D.
Charreau, E.H.
Schillaci, R.
Elizalde, P.V.
Activation of Stat3 by heregulin/ErbB-2 through the co-option of progesterone receptor signaling drives breast cancer growth
topic_facet epidermal growth factor receptor 2
estrogen receptor
neu differentiation factor
progesterone receptor
STAT3 protein
epidermal growth factor receptor 2
neu differentiation factor
progesterone receptor
STAT3 protein
animal cell
animal cell culture
animal experiment
animal model
article
Bagg albino mouse
breast cancer
cancer growth
enzyme activity
female
immunoprecipitation
mouse
nonhuman
priority journal
signal transduction
Western blotting
animal
cell proliferation
experimental neoplasm
metabolism
pathology
Animals
Cell Proliferation
Female
Mammary Neoplasms, Animal
Mice
Mice, Inbred BALB C
Neuregulin-1
Receptor, erbB-2
Receptors, Progesterone
Signal Transduction
STAT3 Transcription Factor
description Cross talk between the steroid hormone receptors for estrogen and progesterone (PR) and the ErbB family of receptor tyrosine kinases appears to be a hallmark of breast cancer growth, but its underlying mechanism remains poorly explored. Here we have highlighted signal transducer and activator of transcription 3 (Stat3) as a key protein activated by heregulin (HRG), a ligand of the ErbB receptors, through co-opted, ligand-independent PR function as a signaling molecule. Stat3 activation was an absolute requirement in HRG-induced mammary tumor growth, and targeting Stat3 effectively inhibited growth of breast cancer cells with activated HRG/ErbB-2 and PR. Our findings unravel a novel potential therapeutic intervention in PR- and ErbB-2-positive breast tumors, involving the specific blockage of PR signaling activity. Copyright © 2009, American Society for Microbiology. All Rights Reserved.
format JOUR
author Proietti, C.J.
Rosemblit, C.
Beguelin, W.
Rivas, M.A.
Flaqué, M.C.D.
Charreau, E.H.
Schillaci, R.
Elizalde, P.V.
author_facet Proietti, C.J.
Rosemblit, C.
Beguelin, W.
Rivas, M.A.
Flaqué, M.C.D.
Charreau, E.H.
Schillaci, R.
Elizalde, P.V.
author_sort Proietti, C.J.
title Activation of Stat3 by heregulin/ErbB-2 through the co-option of progesterone receptor signaling drives breast cancer growth
title_short Activation of Stat3 by heregulin/ErbB-2 through the co-option of progesterone receptor signaling drives breast cancer growth
title_full Activation of Stat3 by heregulin/ErbB-2 through the co-option of progesterone receptor signaling drives breast cancer growth
title_fullStr Activation of Stat3 by heregulin/ErbB-2 through the co-option of progesterone receptor signaling drives breast cancer growth
title_full_unstemmed Activation of Stat3 by heregulin/ErbB-2 through the co-option of progesterone receptor signaling drives breast cancer growth
title_sort activation of stat3 by heregulin/erbb-2 through the co-option of progesterone receptor signaling drives breast cancer growth
url http://hdl.handle.net/20.500.12110/paper_02707306_v29_n5_p1249_Proietti
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