GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models

Autores
Stelitano, Debora; Leticia, Yamila Peche; Dalla, Emiliano; Monte, Martin; Piazza, Silvano; Schneider, Claudio
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Dissemination of cancer cells from the primary tumors to distant organs represents the main cause of death in cancer patients. GTSE1 over-expression has been reported as a potential marker for metastasis in various types of malignancies including breast cancer where GTSE1 expression levels correlate with tumor grade, enhanced invasive potential and negative prognosis. Given the tight correlation between GTSE1 deregulation and bad clinical outcome the aim of this work was to clarify how GTSE1 is regulated in TNBC and the molecular mechanism underlying GTSE1-dependent cell movement. Here, we identified GTSE1 as a novel direct TEAD4 and E2F1 transcription factors target gene highlighting a role for YAP and TAZ co-activators in GTSE1 transcriptional regulation. Frequently deregulated in cancers, TEAD4 and the co-activators YAP and TAZ have been reported to promote tumorigenesis, invasion and metastasis in breast cancer. Here, we demonstrated that the effect of TEAD transcription factor on cell migration and invasion is GTSE1-dependent. Moreover, we found that TEAD controls cell protrusions formation, required for cell migration, through GTSE1 protein unveiling a relevant effector role for GTSE1 in the TEAD-dependent cellular functions.
Fil: Stelitano, Debora. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia
Fil: Leticia, Yamila Peche. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia
Fil: Dalla, Emiliano. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia
Fil: Monte, Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Piazza, Silvano. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia. University of Trento; Italia
Fil: Schneider, Claudio. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia. Università degli Studi di Udine; Italia
Materia
Gtse
Triple Negative Breast Cancer
E2f
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/84422
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/84422
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell modelsStelitano, DeboraLeticia, Yamila PecheDalla, EmilianoMonte, MartinPiazza, SilvanoSchneider, ClaudioGtseTriple Negative Breast CancerE2fhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Dissemination of cancer cells from the primary tumors to distant organs represents the main cause of death in cancer patients. GTSE1 over-expression has been reported as a potential marker for metastasis in various types of malignancies including breast cancer where GTSE1 expression levels correlate with tumor grade, enhanced invasive potential and negative prognosis. Given the tight correlation between GTSE1 deregulation and bad clinical outcome the aim of this work was to clarify how GTSE1 is regulated in TNBC and the molecular mechanism underlying GTSE1-dependent cell movement. Here, we identified GTSE1 as a novel direct TEAD4 and E2F1 transcription factors target gene highlighting a role for YAP and TAZ co-activators in GTSE1 transcriptional regulation. Frequently deregulated in cancers, TEAD4 and the co-activators YAP and TAZ have been reported to promote tumorigenesis, invasion and metastasis in breast cancer. Here, we demonstrated that the effect of TEAD transcription factor on cell migration and invasion is GTSE1-dependent. Moreover, we found that TEAD controls cell protrusions formation, required for cell migration, through GTSE1 protein unveiling a relevant effector role for GTSE1 in the TEAD-dependent cellular functions.Fil: Stelitano, Debora. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; ItaliaFil: Leticia, Yamila Peche. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; ItaliaFil: Dalla, Emiliano. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; ItaliaFil: Monte, Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Piazza, Silvano. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia. University of Trento; ItaliaFil: Schneider, Claudio. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia. Università degli Studi di Udine; ItaliaImpact Journals2017-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/84422Stelitano, Debora; Leticia, Yamila Peche; Dalla, Emiliano; Monte, Martin; Piazza, Silvano; et al.; GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models; Impact Journals; Oncotarget; 8; 40; 6-2017; 67422-674381949-2553CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=18691&path[]=60039info:eu-repo/semantics/altIdentifier/doi/10.18632/oncotarget.18691info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:08:37Zoai:ri.conicet.gov.ar:11336/84422instacron: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 10:08:38.078CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models
title GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models
spellingShingle GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models
Stelitano, Debora
Gtse
Triple Negative Breast Cancer
E2f
title_short GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models
title_full GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models
title_fullStr GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models
title_full_unstemmed GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models
title_sort GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models
dc.creator.none.fl_str_mv Stelitano, Debora
Leticia, Yamila Peche
Dalla, Emiliano
Monte, Martin
Piazza, Silvano
Schneider, Claudio
author Stelitano, Debora
author_facet Stelitano, Debora
Leticia, Yamila Peche
Dalla, Emiliano
Monte, Martin
Piazza, Silvano
Schneider, Claudio
author_role author
author2 Leticia, Yamila Peche
Dalla, Emiliano
Monte, Martin
Piazza, Silvano
Schneider, Claudio
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Gtse
Triple Negative Breast Cancer
E2f
topic Gtse
Triple Negative Breast Cancer
E2f
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Dissemination of cancer cells from the primary tumors to distant organs represents the main cause of death in cancer patients. GTSE1 over-expression has been reported as a potential marker for metastasis in various types of malignancies including breast cancer where GTSE1 expression levels correlate with tumor grade, enhanced invasive potential and negative prognosis. Given the tight correlation between GTSE1 deregulation and bad clinical outcome the aim of this work was to clarify how GTSE1 is regulated in TNBC and the molecular mechanism underlying GTSE1-dependent cell movement. Here, we identified GTSE1 as a novel direct TEAD4 and E2F1 transcription factors target gene highlighting a role for YAP and TAZ co-activators in GTSE1 transcriptional regulation. Frequently deregulated in cancers, TEAD4 and the co-activators YAP and TAZ have been reported to promote tumorigenesis, invasion and metastasis in breast cancer. Here, we demonstrated that the effect of TEAD transcription factor on cell migration and invasion is GTSE1-dependent. Moreover, we found that TEAD controls cell protrusions formation, required for cell migration, through GTSE1 protein unveiling a relevant effector role for GTSE1 in the TEAD-dependent cellular functions.
Fil: Stelitano, Debora. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia
Fil: Leticia, Yamila Peche. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia
Fil: Dalla, Emiliano. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia
Fil: Monte, Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Piazza, Silvano. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia. University of Trento; Italia
Fil: Schneider, Claudio. Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie; Italia. Università degli Studi di Udine; Italia
description Dissemination of cancer cells from the primary tumors to distant organs represents the main cause of death in cancer patients. GTSE1 over-expression has been reported as a potential marker for metastasis in various types of malignancies including breast cancer where GTSE1 expression levels correlate with tumor grade, enhanced invasive potential and negative prognosis. Given the tight correlation between GTSE1 deregulation and bad clinical outcome the aim of this work was to clarify how GTSE1 is regulated in TNBC and the molecular mechanism underlying GTSE1-dependent cell movement. Here, we identified GTSE1 as a novel direct TEAD4 and E2F1 transcription factors target gene highlighting a role for YAP and TAZ co-activators in GTSE1 transcriptional regulation. Frequently deregulated in cancers, TEAD4 and the co-activators YAP and TAZ have been reported to promote tumorigenesis, invasion and metastasis in breast cancer. Here, we demonstrated that the effect of TEAD transcription factor on cell migration and invasion is GTSE1-dependent. Moreover, we found that TEAD controls cell protrusions formation, required for cell migration, through GTSE1 protein unveiling a relevant effector role for GTSE1 in the TEAD-dependent cellular functions.
publishDate 2017
dc.date.none.fl_str_mv 2017-06
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/11336/84422
Stelitano, Debora; Leticia, Yamila Peche; Dalla, Emiliano; Monte, Martin; Piazza, Silvano; et al.; GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models; Impact Journals; Oncotarget; 8; 40; 6-2017; 67422-67438
1949-2553
CONICET Digital
CONICET
url http://hdl.handle.net/11336/84422
identifier_str_mv Stelitano, Debora; Leticia, Yamila Peche; Dalla, Emiliano; Monte, Martin; Piazza, Silvano; et al.; GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models; Impact Journals; Oncotarget; 8; 40; 6-2017; 67422-67438
1949-2553
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=18691&path[]=60039
info:eu-repo/semantics/altIdentifier/doi/10.18632/oncotarget.18691
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Impact Journals
publisher.none.fl_str_mv Impact Journals
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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score 13.13397

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