Estrogen receptor-ID4 cross talk in breast cancer

Autores
Nasif, Daniela Lucía; Roque Moreno, Maria; Branham, Maria Teresita
Año de publicación
2020
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Inhibitor of differentiation (ID) 4, a member of the ID family, has been shown to act as a tumor suppressor and as an oncogene in breast cancer. Our group has investigated this apparent discordant information and has found evidence that ID4 acts as a tumor suppressor only in estrogen receptor ER+ tumors and as an oncogene only in ER- tumors. Here we focus on ID4?s tumor suppressor role and further investigate why ID4 is aberrantly methylated exclusively in ER+ tumors.EZH2 is a histone methyltransferase involved in the tri-methylation of lysine 27 on histone 3 (H3K27me3) and also promotes DNA methylation via DNMT recruitment. In breast cancer EZH2 is overexpressed and downregulates the expression of tumor suppressor genes via increased promoter H3K27me3. Since ID4 is hyper-methylated in ER+ tumors and since EZH2 expression is induced by estradiol we hypothesize that estradiol induces ID4 methylation through EZH2. We performed siRNA (EZH2), immunofluorescence and chromatin immunoprecipitation (CHIP) experiments in MCF7 breast cancer cell lines. Our results show that EZH2 regulates ID4 expression as confirmed by siRNA experiments, that estrogen treatment increases EZH2 expression and ID4 methylation and CHIP experiments reveal that estrogen administration increases EZH2 and H3K27me3 marks on ID4 promoter. Taken together our results show for the first time that estradiol induces ID4 methylation trough EZH2 in breast cancer cell lines.
Fil: Nasif, Daniela Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina
Fil: Roque Moreno, Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina
Fil: Branham, Maria Teresita. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina
LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología
Buenos Aires
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Sociedad Argentina de Fisiología
Materia
ID4
ESTROGEN RECEPTOR
BREAST CANCER
EPIGENETICS
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:11336/188645
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/188645
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Estrogen receptor-ID4 cross talk in breast cancerNasif, Daniela LucíaRoque Moreno, MariaBranham, Maria TeresitaID4ESTROGEN RECEPTORBREAST CANCEREPIGENETICShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Inhibitor of differentiation (ID) 4, a member of the ID family, has been shown to act as a tumor suppressor and as an oncogene in breast cancer. Our group has investigated this apparent discordant information and has found evidence that ID4 acts as a tumor suppressor only in estrogen receptor ER+ tumors and as an oncogene only in ER- tumors. Here we focus on ID4?s tumor suppressor role and further investigate why ID4 is aberrantly methylated exclusively in ER+ tumors.EZH2 is a histone methyltransferase involved in the tri-methylation of lysine 27 on histone 3 (H3K27me3) and also promotes DNA methylation via DNMT recruitment. In breast cancer EZH2 is overexpressed and downregulates the expression of tumor suppressor genes via increased promoter H3K27me3. Since ID4 is hyper-methylated in ER+ tumors and since EZH2 expression is induced by estradiol we hypothesize that estradiol induces ID4 methylation through EZH2. We performed siRNA (EZH2), immunofluorescence and chromatin immunoprecipitation (CHIP) experiments in MCF7 breast cancer cell lines. Our results show that EZH2 regulates ID4 expression as confirmed by siRNA experiments, that estrogen treatment increases EZH2 expression and ID4 methylation and CHIP experiments reveal that estrogen administration increases EZH2 and H3K27me3 marks on ID4 promoter. Taken together our results show for the first time that estradiol induces ID4 methylation trough EZH2 in breast cancer cell lines.Fil: Nasif, Daniela Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Roque Moreno, Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Branham, Maria Teresita. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaLXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de FisiologíaBuenos AiresArgentinaSociedad Argentina de Investigación ClínicaSociedad Argentina de InmunologíaSociedad Argentina de FisiologíaFundación Revista MedicinaCarrillo, CristinaTrevani, Analía SilvinaLarocca, Maria Cecilia2020info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/188645Estrogen receptor-ID4 cross talk in breast cancer; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Buenos Aires; Argentina; 2020; 136-1360025-7680CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.medicinabuenosaires.com/indices-de-2020/Internacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:59:21Zoai:ri.conicet.gov.ar:11336/188645instacron: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 09:59:22.177CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Estrogen receptor-ID4 cross talk in breast cancer
title Estrogen receptor-ID4 cross talk in breast cancer
spellingShingle Estrogen receptor-ID4 cross talk in breast cancer
Nasif, Daniela Lucía
ID4
ESTROGEN RECEPTOR
BREAST CANCER
EPIGENETICS
title_short Estrogen receptor-ID4 cross talk in breast cancer
title_full Estrogen receptor-ID4 cross talk in breast cancer
title_fullStr Estrogen receptor-ID4 cross talk in breast cancer
title_full_unstemmed Estrogen receptor-ID4 cross talk in breast cancer
title_sort Estrogen receptor-ID4 cross talk in breast cancer
dc.creator.none.fl_str_mv Nasif, Daniela Lucía
Roque Moreno, Maria
Branham, Maria Teresita
author Nasif, Daniela Lucía
author_facet Nasif, Daniela Lucía
Roque Moreno, Maria
Branham, Maria Teresita
author_role author
author2 Roque Moreno, Maria
Branham, Maria Teresita
author2_role author
author
dc.contributor.none.fl_str_mv Carrillo, Cristina
Trevani, Analía Silvina
Larocca, Maria Cecilia
dc.subject.none.fl_str_mv ID4
ESTROGEN RECEPTOR
BREAST CANCER
EPIGENETICS
topic ID4
ESTROGEN RECEPTOR
BREAST CANCER
EPIGENETICS
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Inhibitor of differentiation (ID) 4, a member of the ID family, has been shown to act as a tumor suppressor and as an oncogene in breast cancer. Our group has investigated this apparent discordant information and has found evidence that ID4 acts as a tumor suppressor only in estrogen receptor ER+ tumors and as an oncogene only in ER- tumors. Here we focus on ID4?s tumor suppressor role and further investigate why ID4 is aberrantly methylated exclusively in ER+ tumors.EZH2 is a histone methyltransferase involved in the tri-methylation of lysine 27 on histone 3 (H3K27me3) and also promotes DNA methylation via DNMT recruitment. In breast cancer EZH2 is overexpressed and downregulates the expression of tumor suppressor genes via increased promoter H3K27me3. Since ID4 is hyper-methylated in ER+ tumors and since EZH2 expression is induced by estradiol we hypothesize that estradiol induces ID4 methylation through EZH2. We performed siRNA (EZH2), immunofluorescence and chromatin immunoprecipitation (CHIP) experiments in MCF7 breast cancer cell lines. Our results show that EZH2 regulates ID4 expression as confirmed by siRNA experiments, that estrogen treatment increases EZH2 expression and ID4 methylation and CHIP experiments reveal that estrogen administration increases EZH2 and H3K27me3 marks on ID4 promoter. Taken together our results show for the first time that estradiol induces ID4 methylation trough EZH2 in breast cancer cell lines.
Fil: Nasif, Daniela Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina
Fil: Roque Moreno, Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina
Fil: Branham, Maria Teresita. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina
LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología
Buenos Aires
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Sociedad Argentina de Fisiología
description Inhibitor of differentiation (ID) 4, a member of the ID family, has been shown to act as a tumor suppressor and as an oncogene in breast cancer. Our group has investigated this apparent discordant information and has found evidence that ID4 acts as a tumor suppressor only in estrogen receptor ER+ tumors and as an oncogene only in ER- tumors. Here we focus on ID4?s tumor suppressor role and further investigate why ID4 is aberrantly methylated exclusively in ER+ tumors.EZH2 is a histone methyltransferase involved in the tri-methylation of lysine 27 on histone 3 (H3K27me3) and also promotes DNA methylation via DNMT recruitment. In breast cancer EZH2 is overexpressed and downregulates the expression of tumor suppressor genes via increased promoter H3K27me3. Since ID4 is hyper-methylated in ER+ tumors and since EZH2 expression is induced by estradiol we hypothesize that estradiol induces ID4 methylation through EZH2. We performed siRNA (EZH2), immunofluorescence and chromatin immunoprecipitation (CHIP) experiments in MCF7 breast cancer cell lines. Our results show that EZH2 regulates ID4 expression as confirmed by siRNA experiments, that estrogen treatment increases EZH2 expression and ID4 methylation and CHIP experiments reveal that estrogen administration increases EZH2 and H3K27me3 marks on ID4 promoter. Taken together our results show for the first time that estradiol induces ID4 methylation trough EZH2 in breast cancer cell lines.
publishDate 2020
dc.date.none.fl_str_mv 2020
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Reunión
Journal
http://purl.org/coar/resource_type/c_5794
info:ar-repo/semantics/documentoDeConferencia
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/188645
Estrogen receptor-ID4 cross talk in breast cancer; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Buenos Aires; Argentina; 2020; 136-136
0025-7680
CONICET Digital
CONICET
url http://hdl.handle.net/11336/188645
identifier_str_mv Estrogen receptor-ID4 cross talk in breast cancer; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Buenos Aires; Argentina; 2020; 136-136
0025-7680
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.medicinabuenosaires.com/indices-de-2020/
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
dc.coverage.none.fl_str_mv Internacional
dc.publisher.none.fl_str_mv Fundación Revista Medicina
publisher.none.fl_str_mv Fundación Revista Medicina
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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