Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression

Autores
Castillo, Ana Fernanda; Orlando, Ulises Daniel; Lopez, Paula Veronica; Solano, Angela Rosario; Maloberti, Paula Mariana; Podesta, Ernesto Jorge
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Aim: Breast cancer comprises a heterogeneous group of diseases that vary in morphology, biology, behavior and response to therapy. Previous studies have identified an acyl-CoA synthetase 4 (ACSL4) gene-expression pattern correlated with very aggressive tumors. In particular, we have used the tetracycline Tet-Off system to stably transfect non-aggressive breast cancer MCF-7 cells and developed a stable line overexpressing ACSL4 (MCF-7 Tet-Off/ACSL4). As a result, we have proven that cell transfection solely with ACSL4 cDNA renders a highly aggressive phenotype in vitro and results in the development of growing tumors when injected into nude mice. Nevertheless, and in spite of widespread consensus on the role of ACSL4 in mediating an aggressive phenotype in breast cancer, the early steps through which ACSL4 increases tumor growth and progression have been scarcely described and need further elucidation. For this reason, the goal of this work was to study the gene expression profile and the signaling pathways triggered by ACSL4 overexpression in the mechanism that leads to an aggressive phenotype in breast cancer. Methods: We have performed a massive in-depth mRNA sequencing approach and a reverse-phase protein array using MCF-7 Tet-Off/ACSL4 cells as a model to identify gene expression and functional proteomic signatures specific to ACSL4 overexpression. Results and Conclusion: The sole expression of ACSL4 displays a distinctive transcriptome and functional proteomic profile. Furthermore, gene networks most significantly upregulated in breast cancer cells overexpressing ACSL4 are associated to the regulation of embryonic and tissue development, cellular movement and DNA replication and repair. In conclusion, ACSL4 is an upstream regulator of tumorigenic pathways. Because an aggressive tumor phenotype appears in the early stages of metastatic progression, the previously unknown mediators of ACSL4 might.
Fil: Castillo, Ana Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
Fil: Orlando, Ulises Daniel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
Fil: Lopez, Paula Veronica. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
Fil: Solano, Angela Rosario. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
Fil: Maloberti, Paula Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
Fil: Podesta, Ernesto Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
Materia
Acyl-CoA synthetase 4
Breast cancer
Functional proteomics
Transcriptome
Gene signature
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/15298
Acceder
id CONICETDig_e5082aed7545875a99d46524e746630f
oai_identifier_str oai:ri.conicet.gov.ar:11336/15298
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpressionCastillo, Ana FernandaOrlando, Ulises DanielLopez, Paula VeronicaSolano, Angela RosarioMaloberti, Paula MarianaPodesta, Ernesto JorgeAcyl-CoA synthetase 4Breast cancerFunctional proteomicsTranscriptomeGene signaturehttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Aim: Breast cancer comprises a heterogeneous group of diseases that vary in morphology, biology, behavior and response to therapy. Previous studies have identified an acyl-CoA synthetase 4 (ACSL4) gene-expression pattern correlated with very aggressive tumors. In particular, we have used the tetracycline Tet-Off system to stably transfect non-aggressive breast cancer MCF-7 cells and developed a stable line overexpressing ACSL4 (MCF-7 Tet-Off/ACSL4). As a result, we have proven that cell transfection solely with ACSL4 cDNA renders a highly aggressive phenotype in vitro and results in the development of growing tumors when injected into nude mice. Nevertheless, and in spite of widespread consensus on the role of ACSL4 in mediating an aggressive phenotype in breast cancer, the early steps through which ACSL4 increases tumor growth and progression have been scarcely described and need further elucidation. For this reason, the goal of this work was to study the gene expression profile and the signaling pathways triggered by ACSL4 overexpression in the mechanism that leads to an aggressive phenotype in breast cancer. Methods: We have performed a massive in-depth mRNA sequencing approach and a reverse-phase protein array using MCF-7 Tet-Off/ACSL4 cells as a model to identify gene expression and functional proteomic signatures specific to ACSL4 overexpression. Results and Conclusion: The sole expression of ACSL4 displays a distinctive transcriptome and functional proteomic profile. Furthermore, gene networks most significantly upregulated in breast cancer cells overexpressing ACSL4 are associated to the regulation of embryonic and tissue development, cellular movement and DNA replication and repair. In conclusion, ACSL4 is an upstream regulator of tumorigenic pathways. Because an aggressive tumor phenotype appears in the early stages of metastatic progression, the previously unknown mediators of ACSL4 might.Fil: Castillo, Ana Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; ArgentinaFil: Orlando, Ulises Daniel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; ArgentinaFil: Lopez, Paula Veronica. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; ArgentinaFil: Solano, Angela Rosario. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; ArgentinaFil: Maloberti, Paula Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; ArgentinaFil: Podesta, Ernesto Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; ArgentinaOMICS International2015-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/15298Castillo, Ana Fernanda; Orlando, Ulises Daniel; Lopez, Paula Veronica; Solano, Angela Rosario; Maloberti, Paula Mariana; et al.; Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression; OMICS International; Transcriptomics; 3; 2; 11-2015; 1-262329-8936enginfo:eu-repo/semantics/altIdentifier/url/https://www.esciencecentral.org/journals/gene-expression-profile-and-signaling-pathways-in-mcf7-breast-cancercells-mediated-by-acylcoa-synthetase-4-overexpression-2329-8936-1000120.php?aid=65696info:eu-repo/semantics/altIdentifier/doi/10.4172/2329-8936.1000120info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:49:05Zoai:ri.conicet.gov.ar:11336/15298instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:49:05.768CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression
title Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression
spellingShingle Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression
Castillo, Ana Fernanda
Acyl-CoA synthetase 4
Breast cancer
Functional proteomics
Transcriptome
Gene signature
title_short Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression
title_full Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression
title_fullStr Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression
title_full_unstemmed Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression
title_sort Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression
dc.creator.none.fl_str_mv Castillo, Ana Fernanda
Orlando, Ulises Daniel
Lopez, Paula Veronica
Solano, Angela Rosario
Maloberti, Paula Mariana
Podesta, Ernesto Jorge
author Castillo, Ana Fernanda
author_facet Castillo, Ana Fernanda
Orlando, Ulises Daniel
Lopez, Paula Veronica
Solano, Angela Rosario
Maloberti, Paula Mariana
Podesta, Ernesto Jorge
author_role author
author2 Orlando, Ulises Daniel
Lopez, Paula Veronica
Solano, Angela Rosario
Maloberti, Paula Mariana
Podesta, Ernesto Jorge
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Acyl-CoA synthetase 4
Breast cancer
Functional proteomics
Transcriptome
Gene signature
topic Acyl-CoA synthetase 4
Breast cancer
Functional proteomics
Transcriptome
Gene signature
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Aim: Breast cancer comprises a heterogeneous group of diseases that vary in morphology, biology, behavior and response to therapy. Previous studies have identified an acyl-CoA synthetase 4 (ACSL4) gene-expression pattern correlated with very aggressive tumors. In particular, we have used the tetracycline Tet-Off system to stably transfect non-aggressive breast cancer MCF-7 cells and developed a stable line overexpressing ACSL4 (MCF-7 Tet-Off/ACSL4). As a result, we have proven that cell transfection solely with ACSL4 cDNA renders a highly aggressive phenotype in vitro and results in the development of growing tumors when injected into nude mice. Nevertheless, and in spite of widespread consensus on the role of ACSL4 in mediating an aggressive phenotype in breast cancer, the early steps through which ACSL4 increases tumor growth and progression have been scarcely described and need further elucidation. For this reason, the goal of this work was to study the gene expression profile and the signaling pathways triggered by ACSL4 overexpression in the mechanism that leads to an aggressive phenotype in breast cancer. Methods: We have performed a massive in-depth mRNA sequencing approach and a reverse-phase protein array using MCF-7 Tet-Off/ACSL4 cells as a model to identify gene expression and functional proteomic signatures specific to ACSL4 overexpression. Results and Conclusion: The sole expression of ACSL4 displays a distinctive transcriptome and functional proteomic profile. Furthermore, gene networks most significantly upregulated in breast cancer cells overexpressing ACSL4 are associated to the regulation of embryonic and tissue development, cellular movement and DNA replication and repair. In conclusion, ACSL4 is an upstream regulator of tumorigenic pathways. Because an aggressive tumor phenotype appears in the early stages of metastatic progression, the previously unknown mediators of ACSL4 might.
Fil: Castillo, Ana Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
Fil: Orlando, Ulises Daniel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
Fil: Lopez, Paula Veronica. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
Fil: Solano, Angela Rosario. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
Fil: Maloberti, Paula Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
Fil: Podesta, Ernesto Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquimica; Argentina
description Aim: Breast cancer comprises a heterogeneous group of diseases that vary in morphology, biology, behavior and response to therapy. Previous studies have identified an acyl-CoA synthetase 4 (ACSL4) gene-expression pattern correlated with very aggressive tumors. In particular, we have used the tetracycline Tet-Off system to stably transfect non-aggressive breast cancer MCF-7 cells and developed a stable line overexpressing ACSL4 (MCF-7 Tet-Off/ACSL4). As a result, we have proven that cell transfection solely with ACSL4 cDNA renders a highly aggressive phenotype in vitro and results in the development of growing tumors when injected into nude mice. Nevertheless, and in spite of widespread consensus on the role of ACSL4 in mediating an aggressive phenotype in breast cancer, the early steps through which ACSL4 increases tumor growth and progression have been scarcely described and need further elucidation. For this reason, the goal of this work was to study the gene expression profile and the signaling pathways triggered by ACSL4 overexpression in the mechanism that leads to an aggressive phenotype in breast cancer. Methods: We have performed a massive in-depth mRNA sequencing approach and a reverse-phase protein array using MCF-7 Tet-Off/ACSL4 cells as a model to identify gene expression and functional proteomic signatures specific to ACSL4 overexpression. Results and Conclusion: The sole expression of ACSL4 displays a distinctive transcriptome and functional proteomic profile. Furthermore, gene networks most significantly upregulated in breast cancer cells overexpressing ACSL4 are associated to the regulation of embryonic and tissue development, cellular movement and DNA replication and repair. In conclusion, ACSL4 is an upstream regulator of tumorigenic pathways. Because an aggressive tumor phenotype appears in the early stages of metastatic progression, the previously unknown mediators of ACSL4 might.
publishDate 2015
dc.date.none.fl_str_mv 2015-11
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/11336/15298
Castillo, Ana Fernanda; Orlando, Ulises Daniel; Lopez, Paula Veronica; Solano, Angela Rosario; Maloberti, Paula Mariana; et al.; Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression; OMICS International; Transcriptomics; 3; 2; 11-2015; 1-26
2329-8936
url http://hdl.handle.net/11336/15298
identifier_str_mv Castillo, Ana Fernanda; Orlando, Ulises Daniel; Lopez, Paula Veronica; Solano, Angela Rosario; Maloberti, Paula Mariana; et al.; Gene expression profile and signaling pathways in MCF-7 breast cancer cells mediated by acyl-CoA synthetase 4 overexpression; OMICS International; Transcriptomics; 3; 2; 11-2015; 1-26
2329-8936
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.esciencecentral.org/journals/gene-expression-profile-and-signaling-pathways-in-mcf7-breast-cancercells-mediated-by-acylcoa-synthetase-4-overexpression-2329-8936-1000120.php?aid=65696
info:eu-repo/semantics/altIdentifier/doi/10.4172/2329-8936.1000120
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv OMICS International
publisher.none.fl_str_mv OMICS International
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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