Bcl-XL mediates epidermal growth factor dependent cell survival in HC11 mammary epithelial cells

Autores
Romorini, L.; Coso, O.A.; Pecci, A.
Año de publicación
2009
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Apoptosis is the predominant process controlling cell deletion during post-lactational mammary gland remodeling. The members of the Bcl-2 protein family, whose expression levels are under the control of lactogenic hormones, internally control this mechanism. Epidermal growth factor (EGF) belongs to a family of proteins that act as survival factors for mammary epithelial cells upon binding to specific membrane tyrosine kinase receptors. Expression of EGF peaks during lactation and dramatically decreases in the involuting mammary gland. Though it was suggested that the protective effect of EGF is mediated through the phosphatidylinositol-3-kinase (PI3K) or MEK/ERK kinases activities, little is known about the downstream mechanisms involved on the anti-apoptotic effect of EGF on mammary epithelial cells; particularly the identity of target genes controlling apoptosis. Here, we focused on the effect of EGF on the survival of mammary epithelial cells. We particularly aimed at the characterization of the signaling pathways that were triggered by this growth factor, impinge upon expression of Bcl-2 family members and therefore have an impact on the regulation of cell survival. We demonstrate that EGF provokes the induction of the anti-apoptotic isoform Bcl-XL and the phosphorylation and down-regulation of the pro-apoptotic protein Bad. The activation of JNK and PI3K/AKT signaling pathways promotes the induction of Bcl-XL while AKT activation also leads to Bad phosphorylation and down-regulation. This protective effect of EGF correlates mainly with the up-regulation of Bcl-XL than with the down-regulation of Bad. In fact, HC11 cells unable to express bcl-X, die even in the presence of EGF. In this context, Bcl-XL emerges as a key anti-apoptotic molecule critical for mediating EGF cell survival. © 2008 Elsevier B.V. All rights reserved.
Fil:Romorini, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fil:Coso, O.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fil:Pecci, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fuente
Biochim. Biophys. Acta Mol. Cell Res. 2009;1793(3):496-505
Materia
Apoptosis
Bad
Bcl-XL
EGF
Mammary epithelial cell
MAPKs
cytochrome c
mitogen activated protein kinase 1
mitogen activated protein kinase 3
phosphatidylinositol 3 kinase
protein BAD
protein bcl 2
protein bcl xl
protein kinase B
recombinant epidermal growth factor
stress activated protein kinase
cytochrome c
epidermal growth factor
phosphatidylinositol 3 kinase
protein BAD
protein bcl x
protein kinase B
stress activated protein kinase
animal cell
apoptosis
article
breast epithelium
cell survival
controlled study
down regulation
enzyme activation
epithelium cell
mitochondrion
mouse
nonhuman
priority journal
protein expression
protein family
protein induction
protein phosphorylation
protein secretion
signal transduction
animal
cell survival
epithelium cell
female
genetics
human
metabolism
phosphorylation
udder
1-Phosphatidylinositol 3-Kinase
Animals
Apoptosis
bcl-Associated Death Protein
bcl-X Protein
Cell Survival
Cytochromes c
Down-Regulation
Epidermal Growth Factor
Epithelial Cells
Female
Humans
JNK Mitogen-Activated Protein Kinases
Mammary Glands, Animal
Mice
Mitochondria
Phosphorylation
Proto-Oncogene Proteins c-akt
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/2.5/ar
Repositorio
Biblioteca Digital (UBA-FCEN)
Institución
Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
OAI Identificador
paperaa:paper_01674889_v1793_n3_p496_Romorini

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oai_identifier_str paperaa:paper_01674889_v1793_n3_p496_Romorini
network_acronym_str BDUBAFCEN
repository_id_str 1896
network_name_str Biblioteca Digital (UBA-FCEN)
spelling Bcl-XL mediates epidermal growth factor dependent cell survival in HC11 mammary epithelial cellsRomorini, L.Coso, O.A.Pecci, A.ApoptosisBadBcl-XLEGFMammary epithelial cellMAPKscytochrome cmitogen activated protein kinase 1mitogen activated protein kinase 3phosphatidylinositol 3 kinaseprotein BADprotein bcl 2protein bcl xlprotein kinase Brecombinant epidermal growth factorstress activated protein kinasecytochrome cepidermal growth factorphosphatidylinositol 3 kinaseprotein BADprotein bcl xprotein kinase Bstress activated protein kinaseanimal cellapoptosisarticlebreast epitheliumcell survivalcontrolled studydown regulationenzyme activationepithelium cellmitochondrionmousenonhumanpriority journalprotein expressionprotein familyprotein inductionprotein phosphorylationprotein secretionsignal transductionanimalcell survivalepithelium cellfemalegeneticshumanmetabolismphosphorylationudder1-Phosphatidylinositol 3-KinaseAnimalsApoptosisbcl-Associated Death Proteinbcl-X ProteinCell SurvivalCytochromes cDown-RegulationEpidermal Growth FactorEpithelial CellsFemaleHumansJNK Mitogen-Activated Protein KinasesMammary Glands, AnimalMiceMitochondriaPhosphorylationProto-Oncogene Proteins c-aktApoptosis is the predominant process controlling cell deletion during post-lactational mammary gland remodeling. The members of the Bcl-2 protein family, whose expression levels are under the control of lactogenic hormones, internally control this mechanism. Epidermal growth factor (EGF) belongs to a family of proteins that act as survival factors for mammary epithelial cells upon binding to specific membrane tyrosine kinase receptors. Expression of EGF peaks during lactation and dramatically decreases in the involuting mammary gland. Though it was suggested that the protective effect of EGF is mediated through the phosphatidylinositol-3-kinase (PI3K) or MEK/ERK kinases activities, little is known about the downstream mechanisms involved on the anti-apoptotic effect of EGF on mammary epithelial cells; particularly the identity of target genes controlling apoptosis. Here, we focused on the effect of EGF on the survival of mammary epithelial cells. We particularly aimed at the characterization of the signaling pathways that were triggered by this growth factor, impinge upon expression of Bcl-2 family members and therefore have an impact on the regulation of cell survival. We demonstrate that EGF provokes the induction of the anti-apoptotic isoform Bcl-XL and the phosphorylation and down-regulation of the pro-apoptotic protein Bad. The activation of JNK and PI3K/AKT signaling pathways promotes the induction of Bcl-XL while AKT activation also leads to Bad phosphorylation and down-regulation. This protective effect of EGF correlates mainly with the up-regulation of Bcl-XL than with the down-regulation of Bad. In fact, HC11 cells unable to express bcl-X, die even in the presence of EGF. In this context, Bcl-XL emerges as a key anti-apoptotic molecule critical for mediating EGF cell survival. © 2008 Elsevier B.V. All rights reserved.Fil:Romorini, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.Fil:Coso, O.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.Fil:Pecci, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.2009info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://hdl.handle.net/20.500.12110/paper_01674889_v1793_n3_p496_RomoriniBiochim. Biophys. Acta Mol. Cell Res. 2009;1793(3):496-505reponame:Biblioteca Digital (UBA-FCEN)instname:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturalesinstacron:UBA-FCENenginfo:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/2.5/ar2025-09-29T13:42:51Zpaperaa:paper_01674889_v1793_n3_p496_RomoriniInstitucionalhttps://digital.bl.fcen.uba.ar/Universidad públicaNo correspondehttps://digital.bl.fcen.uba.ar/cgi-bin/oaiserver.cgiana@bl.fcen.uba.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:18962025-09-29 13:42:53.167Biblioteca Digital (UBA-FCEN) - Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturalesfalse
dc.title.none.fl_str_mv Bcl-XL mediates epidermal growth factor dependent cell survival in HC11 mammary epithelial cells
title Bcl-XL mediates epidermal growth factor dependent cell survival in HC11 mammary epithelial cells
spellingShingle Bcl-XL mediates epidermal growth factor dependent cell survival in HC11 mammary epithelial cells
Romorini, L.
Apoptosis
Bad
Bcl-XL
EGF
Mammary epithelial cell
MAPKs
cytochrome c
mitogen activated protein kinase 1
mitogen activated protein kinase 3
phosphatidylinositol 3 kinase
protein BAD
protein bcl 2
protein bcl xl
protein kinase B
recombinant epidermal growth factor
stress activated protein kinase
cytochrome c
epidermal growth factor
phosphatidylinositol 3 kinase
protein BAD
protein bcl x
protein kinase B
stress activated protein kinase
animal cell
apoptosis
article
breast epithelium
cell survival
controlled study
down regulation
enzyme activation
epithelium cell
mitochondrion
mouse
nonhuman
priority journal
protein expression
protein family
protein induction
protein phosphorylation
protein secretion
signal transduction
animal
cell survival
epithelium cell
female
genetics
human
metabolism
phosphorylation
udder
1-Phosphatidylinositol 3-Kinase
Animals
Apoptosis
bcl-Associated Death Protein
bcl-X Protein
Cell Survival
Cytochromes c
Down-Regulation
Epidermal Growth Factor
Epithelial Cells
Female
Humans
JNK Mitogen-Activated Protein Kinases
Mammary Glands, Animal
Mice
Mitochondria
Phosphorylation
Proto-Oncogene Proteins c-akt
title_short Bcl-XL mediates epidermal growth factor dependent cell survival in HC11 mammary epithelial cells
title_full Bcl-XL mediates epidermal growth factor dependent cell survival in HC11 mammary epithelial cells
title_fullStr Bcl-XL mediates epidermal growth factor dependent cell survival in HC11 mammary epithelial cells
title_full_unstemmed Bcl-XL mediates epidermal growth factor dependent cell survival in HC11 mammary epithelial cells
title_sort Bcl-XL mediates epidermal growth factor dependent cell survival in HC11 mammary epithelial cells
dc.creator.none.fl_str_mv Romorini, L.
Coso, O.A.
Pecci, A.
author Romorini, L.
author_facet Romorini, L.
Coso, O.A.
Pecci, A.
author_role author
author2 Coso, O.A.
Pecci, A.
author2_role author
author
dc.subject.none.fl_str_mv Apoptosis
Bad
Bcl-XL
EGF
Mammary epithelial cell
MAPKs
cytochrome c
mitogen activated protein kinase 1
mitogen activated protein kinase 3
phosphatidylinositol 3 kinase
protein BAD
protein bcl 2
protein bcl xl
protein kinase B
recombinant epidermal growth factor
stress activated protein kinase
cytochrome c
epidermal growth factor
phosphatidylinositol 3 kinase
protein BAD
protein bcl x
protein kinase B
stress activated protein kinase
animal cell
apoptosis
article
breast epithelium
cell survival
controlled study
down regulation
enzyme activation
epithelium cell
mitochondrion
mouse
nonhuman
priority journal
protein expression
protein family
protein induction
protein phosphorylation
protein secretion
signal transduction
animal
cell survival
epithelium cell
female
genetics
human
metabolism
phosphorylation
udder
1-Phosphatidylinositol 3-Kinase
Animals
Apoptosis
bcl-Associated Death Protein
bcl-X Protein
Cell Survival
Cytochromes c
Down-Regulation
Epidermal Growth Factor
Epithelial Cells
Female
Humans
JNK Mitogen-Activated Protein Kinases
Mammary Glands, Animal
Mice
Mitochondria
Phosphorylation
Proto-Oncogene Proteins c-akt
topic Apoptosis
Bad
Bcl-XL
EGF
Mammary epithelial cell
MAPKs
cytochrome c
mitogen activated protein kinase 1
mitogen activated protein kinase 3
phosphatidylinositol 3 kinase
protein BAD
protein bcl 2
protein bcl xl
protein kinase B
recombinant epidermal growth factor
stress activated protein kinase
cytochrome c
epidermal growth factor
phosphatidylinositol 3 kinase
protein BAD
protein bcl x
protein kinase B
stress activated protein kinase
animal cell
apoptosis
article
breast epithelium
cell survival
controlled study
down regulation
enzyme activation
epithelium cell
mitochondrion
mouse
nonhuman
priority journal
protein expression
protein family
protein induction
protein phosphorylation
protein secretion
signal transduction
animal
cell survival
epithelium cell
female
genetics
human
metabolism
phosphorylation
udder
1-Phosphatidylinositol 3-Kinase
Animals
Apoptosis
bcl-Associated Death Protein
bcl-X Protein
Cell Survival
Cytochromes c
Down-Regulation
Epidermal Growth Factor
Epithelial Cells
Female
Humans
JNK Mitogen-Activated Protein Kinases
Mammary Glands, Animal
Mice
Mitochondria
Phosphorylation
Proto-Oncogene Proteins c-akt
dc.description.none.fl_txt_mv Apoptosis is the predominant process controlling cell deletion during post-lactational mammary gland remodeling. The members of the Bcl-2 protein family, whose expression levels are under the control of lactogenic hormones, internally control this mechanism. Epidermal growth factor (EGF) belongs to a family of proteins that act as survival factors for mammary epithelial cells upon binding to specific membrane tyrosine kinase receptors. Expression of EGF peaks during lactation and dramatically decreases in the involuting mammary gland. Though it was suggested that the protective effect of EGF is mediated through the phosphatidylinositol-3-kinase (PI3K) or MEK/ERK kinases activities, little is known about the downstream mechanisms involved on the anti-apoptotic effect of EGF on mammary epithelial cells; particularly the identity of target genes controlling apoptosis. Here, we focused on the effect of EGF on the survival of mammary epithelial cells. We particularly aimed at the characterization of the signaling pathways that were triggered by this growth factor, impinge upon expression of Bcl-2 family members and therefore have an impact on the regulation of cell survival. We demonstrate that EGF provokes the induction of the anti-apoptotic isoform Bcl-XL and the phosphorylation and down-regulation of the pro-apoptotic protein Bad. The activation of JNK and PI3K/AKT signaling pathways promotes the induction of Bcl-XL while AKT activation also leads to Bad phosphorylation and down-regulation. This protective effect of EGF correlates mainly with the up-regulation of Bcl-XL than with the down-regulation of Bad. In fact, HC11 cells unable to express bcl-X, die even in the presence of EGF. In this context, Bcl-XL emerges as a key anti-apoptotic molecule critical for mediating EGF cell survival. © 2008 Elsevier B.V. All rights reserved.
Fil:Romorini, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fil:Coso, O.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fil:Pecci, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
description Apoptosis is the predominant process controlling cell deletion during post-lactational mammary gland remodeling. The members of the Bcl-2 protein family, whose expression levels are under the control of lactogenic hormones, internally control this mechanism. Epidermal growth factor (EGF) belongs to a family of proteins that act as survival factors for mammary epithelial cells upon binding to specific membrane tyrosine kinase receptors. Expression of EGF peaks during lactation and dramatically decreases in the involuting mammary gland. Though it was suggested that the protective effect of EGF is mediated through the phosphatidylinositol-3-kinase (PI3K) or MEK/ERK kinases activities, little is known about the downstream mechanisms involved on the anti-apoptotic effect of EGF on mammary epithelial cells; particularly the identity of target genes controlling apoptosis. Here, we focused on the effect of EGF on the survival of mammary epithelial cells. We particularly aimed at the characterization of the signaling pathways that were triggered by this growth factor, impinge upon expression of Bcl-2 family members and therefore have an impact on the regulation of cell survival. We demonstrate that EGF provokes the induction of the anti-apoptotic isoform Bcl-XL and the phosphorylation and down-regulation of the pro-apoptotic protein Bad. The activation of JNK and PI3K/AKT signaling pathways promotes the induction of Bcl-XL while AKT activation also leads to Bad phosphorylation and down-regulation. This protective effect of EGF correlates mainly with the up-regulation of Bcl-XL than with the down-regulation of Bad. In fact, HC11 cells unable to express bcl-X, die even in the presence of EGF. In this context, Bcl-XL emerges as a key anti-apoptotic molecule critical for mediating EGF cell survival. © 2008 Elsevier B.V. All rights reserved.
publishDate 2009
dc.date.none.fl_str_mv 2009
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/20.500.12110/paper_01674889_v1793_n3_p496_Romorini
url http://hdl.handle.net/20.500.12110/paper_01674889_v1793_n3_p496_Romorini
dc.language.none.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/2.5/ar
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/2.5/ar
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv Biochim. Biophys. Acta Mol. Cell Res. 2009;1793(3):496-505
reponame:Biblioteca Digital (UBA-FCEN)
instname:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
instacron:UBA-FCEN
reponame_str Biblioteca Digital (UBA-FCEN)
collection Biblioteca Digital (UBA-FCEN)
instname_str Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
instacron_str UBA-FCEN
institution UBA-FCEN
repository.name.fl_str_mv Biblioteca Digital (UBA-FCEN) - Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
repository.mail.fl_str_mv ana@bl.fcen.uba.ar
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