Estrogen receptor beta displays cell cycle-dependent expression and regulates the G1 phase through a non-genomic mechanism in prostate carcinoma cells
Background: It is well known that estrogens regulate cell cycle progression, but the specific contributions and mechanisms of action of the estrogen receptor beta (ERβ) remain elusive. Methods: We have analyzed the levels of ERβ1 and ERβ2 throughout the cell cycle, as well as the mechanisms of actio...
| Autores: | , , , , , , , , , , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2008 |
| País: | España |
| Institución: | Consejo Superior de Investigaciones Científicas (CSIC) |
| Repositorio: | DIGITAL.CSIC. Repositorio Institucional del CSIC |
| OAI Identifier: | oai:digital.csic.es:10261/414660 |
| Acceso en línea: | http://hdl.handle.net/10261/414660 https://api.elsevier.com/content/abstract/scopus_id/47749124288 |
| Access Level: | acceso abierto |
| Palabra clave: | AP1 Cell cycle ERβ1 ERβ2 ERE ICI 182,780 LNCaP |
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Estrogen receptor beta displays cell cycle-dependent expression and regulates the G1 phase through a non-genomic mechanism in prostate carcinoma cellsHurtado, AntoniPinós, TomàsBarbosa-Desongles, AnnaLópez-Avilés, SandraBarquinero, JordiPetriz, JordiSantamaria-Martínez, AlbertMorote, Joande Torres, InésBellmunt, JoaquimReventós, JaumeMunell, FrancinaAP1Cell cycleERβ1ERβ2EREICI 182,780LNCaPBackground: It is well known that estrogens regulate cell cycle progression, but the specific contributions and mechanisms of action of the estrogen receptor beta (ERβ) remain elusive. Methods: We have analyzed the levels of ERβ1 and ERβ2 throughout the cell cycle, as well as the mechanisms of action and the consequences of the over-expression of ERβ1 in the human prostate cancer LNCaP cell line. Results: Both ERβ1 mRNA and protein expression increased from the G1 to the S phase and decreased before entering the G2/M phase, whereas ERβ2 levels decreased during the S phase and increased in the G2/M phase. ERβ1 protein was detected in both the nuclear and non-nuclear fractions, and ERβ2 was found exclusively in the nucleus. Regarding the mechanisms of action, endogenous ERβ was able to activate transcription via ERE during the S phase in a ligand-dependent manner, whereas no changes in AP1 and NFκB transactivation were observed after exposure to estradiol or the specific inhibitor ICI 182,780. Over-expression of either wild type ERβ1 or ERβ1 mutated in the DNA-binding domain caused an arrest in early G1. This arrest was accompanied by the interaction of over-expressed ERβ1 with c-Jun N-terminal protein kinase 1 (JNK1) and a decrease in c-Jun phosphorylation and cyclin D1 expression. The administration of ICI impeded the JNK1–ERβ1 interaction, increased c-Jun phosphorylation and cyclin D1 expression and allowed the cells to progress to late G1, where they became arrested. Conclusions: Our results demonstrate that, in LNCaP prostate cancer cells, both ERβ isoforms are differentially expressed during the cell cycle and that ERβ regulates the G1 phase by a non-genomic mechanism.This work was supported by grants from the Ministerio de Educación y Ciencia (PM 1999-0134), theMinisterio de Sanidad y Consumo (PI020772) and theFundación para la Investigación en Urología. The au-thors would like to thank Alex Bote (UCTS, Hospi-tal Vall d’Hebrón, Barcelona, Spain), Jaume Comas(Serveis Cientifico-Tècnics, Universitat de Barcelona,Barcelona, Spain), and Antoni Iborra (IBB, Universi-tat Autònoma de Barcelona, Bellaterra, Spain) for theirtechnical assistance, Rosa Aligué and Miguel Abal forher technical and scientific support, as well as Lisa Pic-cione, Alfons Macaya and Jason S. Carroll for correc-tion of the manuscriptPeer reviewedJohn Wiley & SonsIOS PressMinisterio de Educación y Ciencia (España)Ministerio de Sanidad y Consumo (España)Fundación Para la Investigación en Urología202620262008info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_6501Publisher's versioninfo:eu-repo/semantics/publishedVersionapplication/pdfhttp://hdl.handle.net/10261/414660https://api.elsevier.com/content/abstract/scopus_id/47749124288reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)Ingléshttps://doi.org/10.3233/CLO-2008-0430Digital Object Identifier (DOI)Noinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/4146602026-05-22T06:33:51Z |
| dc.title.none.fl_str_mv |
Estrogen receptor beta displays cell cycle-dependent expression and regulates the G1 phase through a non-genomic mechanism in prostate carcinoma cells |
| title |
Estrogen receptor beta displays cell cycle-dependent expression and regulates the G1 phase through a non-genomic mechanism in prostate carcinoma cells |
| spellingShingle |
Estrogen receptor beta displays cell cycle-dependent expression and regulates the G1 phase through a non-genomic mechanism in prostate carcinoma cells Hurtado, Antoni AP1 Cell cycle ERβ1 ERβ2 ERE ICI 182,780 LNCaP |
| title_short |
Estrogen receptor beta displays cell cycle-dependent expression and regulates the G1 phase through a non-genomic mechanism in prostate carcinoma cells |
| title_full |
Estrogen receptor beta displays cell cycle-dependent expression and regulates the G1 phase through a non-genomic mechanism in prostate carcinoma cells |
| title_fullStr |
Estrogen receptor beta displays cell cycle-dependent expression and regulates the G1 phase through a non-genomic mechanism in prostate carcinoma cells |
| title_full_unstemmed |
Estrogen receptor beta displays cell cycle-dependent expression and regulates the G1 phase through a non-genomic mechanism in prostate carcinoma cells |
| title_sort |
Estrogen receptor beta displays cell cycle-dependent expression and regulates the G1 phase through a non-genomic mechanism in prostate carcinoma cells |
| dc.creator.none.fl_str_mv |
Hurtado, Antoni Pinós, Tomàs Barbosa-Desongles, Anna López-Avilés, Sandra Barquinero, Jordi Petriz, Jordi Santamaria-Martínez, Albert Morote, Joan de Torres, Inés Bellmunt, Joaquim Reventós, Jaume Munell, Francina |
| author |
Hurtado, Antoni |
| author_facet |
Hurtado, Antoni Pinós, Tomàs Barbosa-Desongles, Anna López-Avilés, Sandra Barquinero, Jordi Petriz, Jordi Santamaria-Martínez, Albert Morote, Joan de Torres, Inés Bellmunt, Joaquim Reventós, Jaume Munell, Francina |
| author_role |
author |
| author2 |
Pinós, Tomàs Barbosa-Desongles, Anna López-Avilés, Sandra Barquinero, Jordi Petriz, Jordi Santamaria-Martínez, Albert Morote, Joan de Torres, Inés Bellmunt, Joaquim Reventós, Jaume Munell, Francina |
| author2_role |
author author author author author author author author author author author |
| dc.contributor.none.fl_str_mv |
Ministerio de Educación y Ciencia (España) Ministerio de Sanidad y Consumo (España) Fundación Para la Investigación en Urología |
| dc.subject.none.fl_str_mv |
AP1 Cell cycle ERβ1 ERβ2 ERE ICI 182,780 LNCaP |
| topic |
AP1 Cell cycle ERβ1 ERβ2 ERE ICI 182,780 LNCaP |
| description |
Background: It is well known that estrogens regulate cell cycle progression, but the specific contributions and mechanisms of action of the estrogen receptor beta (ERβ) remain elusive. Methods: We have analyzed the levels of ERβ1 and ERβ2 throughout the cell cycle, as well as the mechanisms of action and the consequences of the over-expression of ERβ1 in the human prostate cancer LNCaP cell line. Results: Both ERβ1 mRNA and protein expression increased from the G1 to the S phase and decreased before entering the G2/M phase, whereas ERβ2 levels decreased during the S phase and increased in the G2/M phase. ERβ1 protein was detected in both the nuclear and non-nuclear fractions, and ERβ2 was found exclusively in the nucleus. Regarding the mechanisms of action, endogenous ERβ was able to activate transcription via ERE during the S phase in a ligand-dependent manner, whereas no changes in AP1 and NFκB transactivation were observed after exposure to estradiol or the specific inhibitor ICI 182,780. Over-expression of either wild type ERβ1 or ERβ1 mutated in the DNA-binding domain caused an arrest in early G1. This arrest was accompanied by the interaction of over-expressed ERβ1 with c-Jun N-terminal protein kinase 1 (JNK1) and a decrease in c-Jun phosphorylation and cyclin D1 expression. The administration of ICI impeded the JNK1–ERβ1 interaction, increased c-Jun phosphorylation and cyclin D1 expression and allowed the cells to progress to late G1, where they became arrested. Conclusions: Our results demonstrate that, in LNCaP prostate cancer cells, both ERβ isoforms are differentially expressed during the cell cycle and that ERβ regulates the G1 phase by a non-genomic mechanism. |
| publishDate |
2008 |
| dc.date.none.fl_str_mv |
2008 2026 2026 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article http://purl.org/coar/resource_type/c_6501 Publisher's version info:eu-repo/semantics/publishedVersion |
| format |
article |
| status_str |
publishedVersion |
| dc.identifier.none.fl_str_mv |
http://hdl.handle.net/10261/414660 https://api.elsevier.com/content/abstract/scopus_id/47749124288 |
| url |
http://hdl.handle.net/10261/414660 https://api.elsevier.com/content/abstract/scopus_id/47749124288 |
| dc.language.none.fl_str_mv |
Inglés |
| language_invalid_str_mv |
Inglés |
| dc.relation.none.fl_str_mv |
https://doi.org/10.3233/CLO-2008-0430Digital Object Identifier (DOI) No |
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info:eu-repo/semantics/openAccess |
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openAccess |
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application/pdf |
| dc.publisher.none.fl_str_mv |
John Wiley & Sons IOS Press |
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John Wiley & Sons IOS Press |
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reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC instname:Consejo Superior de Investigaciones Científicas (CSIC) |
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Consejo Superior de Investigaciones Científicas (CSIC) |
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DIGITAL.CSIC. Repositorio Institucional del CSIC |
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DIGITAL.CSIC. Repositorio Institucional del CSIC |
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1869419310732017664 |
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15.812429 |