FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences
- Autores
- Giulianelli, Sebastian Jesus; Riggio, Marina; Guillardoy, Tomás; Pérez Piñero, Cecilia; Gorostiaga, María A.; Sequeira, Gonzalo Ricardo; Pataccini, Gabriela; Abascal, María F.; Toledo, María Florencia; Jacobsen, Britta M.; Guerreiro, Ana C.; Barros, António; Novaro, Virginia; Monteiro, Fátima L.; Amado, Francisco; Gass, Hugo; Abba, Martin; Helguero, Luisa A.; Lanari, Claudia
- Año de publicación
- 2019
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Progression to hormone-independent growth leading to endocrine therapy resistance occurs in a high proportion of patients with estrogen receptor alpha (ERα) and progesterone receptors (PR) positive breast cancer. We and others have previously shown that estrogen- and progestin-induced tumor growth requires ERα and PR interaction at their target genes. Here, we show that fibroblast growth factor 2 (FGF2)-induces cell proliferation and tumor growth through hormone-independent ERα and PR activation and their interaction at the MYC enhancer and proximal promoter. MYC inhibitors, antiestrogens or antiprogestins reverted FGF2-induced effects. LC?MS/MS identified 700 canonical proteins recruited to MYC regulatory sequences after FGF2 stimulation, 397 of which required active ERα (ERα-dependent). We identified ERα-dependent proteins regulating transcription that, after FGF2 treatment, were recruited to the enhancer as well as proteins involved in transcription initiation that were recruited to the proximal promoter. Also, among the ERα-dependent and independent proteins detected at both sites, PR isoforms A and B as well as the novel protein product PRBΔ4 were found. PRBΔ4 lacks the hormone-binding domain and was able to induce reporter gene expression from estrogen-regulated elements and to increase cell proliferation when cells were stimulated with FGF2 but not by progestins. Analysis of the Cancer Genome Atlas data set revealed that PRBΔ4 expression is associated with worse overall survival in luminal breast cancer patients. This discovery provides a new mechanism by which growth factor signaling can engage nonclassical hormone receptor isoforms such as PRBΔ4, which interacts with growth-factor activated ERα and PR to stimulate MYC gene expression and hence progression to endocrine resistance.
Fil: Giulianelli, Sebastian Jesus. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Centro Nacional Patagónico. Instituto de Biología de Organismos Marinos; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Riggio, Marina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Guillardoy, Tomás. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Pérez Piñero, Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Gorostiaga, María A.. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Sequeira, Gonzalo Ricardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Pataccini, Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Abascal, María F.. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Toledo, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Jacobsen, Britta M.. University of Colorado; Estados Unidos
Fil: Guerreiro, Ana C.. Universidade de Aveiro; Portugal
Fil: Barros, António. Universidade de Aveiro; Portugal
Fil: Novaro, Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Monteiro, Fátima L.. Universidade de Aveiro; Portugal
Fil: Amado, Francisco. Universidade de Aveiro; Portugal
Fil: Gass, Hugo. Hospital Zonal General de Agudos Magdalena V de Martínez; Argentina
Fil: Abba, Martin. Universidad Nacional de La Plata; Argentina
Fil: Helguero, Luisa A.. Universidade de Aveiro; Portugal
Fil: Lanari, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina - Materia
-
BREAST CANCER
FGF2
HORMONE RECEPTOR INTERACTIONS
MYC
PR ISOFORMS
PRB∆4 - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/107597
Ver los metadatos del registro completo
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FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory SequencesGiulianelli, Sebastian JesusRiggio, MarinaGuillardoy, TomásPérez Piñero, CeciliaGorostiaga, María A.Sequeira, Gonzalo RicardoPataccini, GabrielaAbascal, María F.Toledo, María FlorenciaJacobsen, Britta M.Guerreiro, Ana C.Barros, AntónioNovaro, VirginiaMonteiro, Fátima L.Amado, FranciscoGass, HugoAbba, MartinHelguero, Luisa A.Lanari, ClaudiaBREAST CANCERFGF2HORMONE RECEPTOR INTERACTIONSMYCPR ISOFORMSPRB∆4https://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Progression to hormone-independent growth leading to endocrine therapy resistance occurs in a high proportion of patients with estrogen receptor alpha (ERα) and progesterone receptors (PR) positive breast cancer. We and others have previously shown that estrogen- and progestin-induced tumor growth requires ERα and PR interaction at their target genes. Here, we show that fibroblast growth factor 2 (FGF2)-induces cell proliferation and tumor growth through hormone-independent ERα and PR activation and their interaction at the MYC enhancer and proximal promoter. MYC inhibitors, antiestrogens or antiprogestins reverted FGF2-induced effects. LC?MS/MS identified 700 canonical proteins recruited to MYC regulatory sequences after FGF2 stimulation, 397 of which required active ERα (ERα-dependent). We identified ERα-dependent proteins regulating transcription that, after FGF2 treatment, were recruited to the enhancer as well as proteins involved in transcription initiation that were recruited to the proximal promoter. Also, among the ERα-dependent and independent proteins detected at both sites, PR isoforms A and B as well as the novel protein product PRBΔ4 were found. PRBΔ4 lacks the hormone-binding domain and was able to induce reporter gene expression from estrogen-regulated elements and to increase cell proliferation when cells were stimulated with FGF2 but not by progestins. Analysis of the Cancer Genome Atlas data set revealed that PRBΔ4 expression is associated with worse overall survival in luminal breast cancer patients. This discovery provides a new mechanism by which growth factor signaling can engage nonclassical hormone receptor isoforms such as PRBΔ4, which interacts with growth-factor activated ERα and PR to stimulate MYC gene expression and hence progression to endocrine resistance.Fil: Giulianelli, Sebastian Jesus. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Centro Nacional Patagónico. Instituto de Biología de Organismos Marinos; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Riggio, Marina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Guillardoy, Tomás. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Pérez Piñero, Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Gorostiaga, María A.. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Sequeira, Gonzalo Ricardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Pataccini, Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Abascal, María F.. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Toledo, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Jacobsen, Britta M.. University of Colorado; Estados UnidosFil: Guerreiro, Ana C.. Universidade de Aveiro; PortugalFil: Barros, António. Universidade de Aveiro; PortugalFil: Novaro, Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Monteiro, Fátima L.. Universidade de Aveiro; PortugalFil: Amado, Francisco. Universidade de Aveiro; PortugalFil: Gass, Hugo. Hospital Zonal General de Agudos Magdalena V de Martínez; ArgentinaFil: Abba, Martin. Universidad Nacional de La Plata; ArgentinaFil: Helguero, Luisa A.. Universidade de Aveiro; PortugalFil: Lanari, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaJohn Wiley & Sons Inc2019-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/107597Giulianelli, Sebastian Jesus; Riggio, Marina; Guillardoy, Tomás; Pérez Piñero, Cecilia; Gorostiaga, María A.; et al.; FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences; John Wiley & Sons Inc; International Journal of Cancer; 145; 7; 3-2019; 1874-18880020-71361097-0215CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1002/ijc.32252info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:51:05Zoai:ri.conicet.gov.ar:11336/107597instacron: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 09:51:05.808CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences |
| title |
FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences |
| spellingShingle |
FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences Giulianelli, Sebastian Jesus BREAST CANCER FGF2 HORMONE RECEPTOR INTERACTIONS MYC PR ISOFORMS PRB∆4 |
| title_short |
FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences |
| title_full |
FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences |
| title_fullStr |
FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences |
| title_full_unstemmed |
FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences |
| title_sort |
FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences |
| dc.creator.none.fl_str_mv |
Giulianelli, Sebastian Jesus Riggio, Marina Guillardoy, Tomás Pérez Piñero, Cecilia Gorostiaga, María A. Sequeira, Gonzalo Ricardo Pataccini, Gabriela Abascal, María F. Toledo, María Florencia Jacobsen, Britta M. Guerreiro, Ana C. Barros, António Novaro, Virginia Monteiro, Fátima L. Amado, Francisco Gass, Hugo Abba, Martin Helguero, Luisa A. Lanari, Claudia |
| author |
Giulianelli, Sebastian Jesus |
| author_facet |
Giulianelli, Sebastian Jesus Riggio, Marina Guillardoy, Tomás Pérez Piñero, Cecilia Gorostiaga, María A. Sequeira, Gonzalo Ricardo Pataccini, Gabriela Abascal, María F. Toledo, María Florencia Jacobsen, Britta M. Guerreiro, Ana C. Barros, António Novaro, Virginia Monteiro, Fátima L. Amado, Francisco Gass, Hugo Abba, Martin Helguero, Luisa A. Lanari, Claudia |
| author_role |
author |
| author2 |
Riggio, Marina Guillardoy, Tomás Pérez Piñero, Cecilia Gorostiaga, María A. Sequeira, Gonzalo Ricardo Pataccini, Gabriela Abascal, María F. Toledo, María Florencia Jacobsen, Britta M. Guerreiro, Ana C. Barros, António Novaro, Virginia Monteiro, Fátima L. Amado, Francisco Gass, Hugo Abba, Martin Helguero, Luisa A. Lanari, Claudia |
| author2_role |
author author author author author author author author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
BREAST CANCER FGF2 HORMONE RECEPTOR INTERACTIONS MYC PR ISOFORMS PRB∆4 |
| topic |
BREAST CANCER FGF2 HORMONE RECEPTOR INTERACTIONS MYC PR ISOFORMS PRB∆4 |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| dc.description.none.fl_txt_mv |
Progression to hormone-independent growth leading to endocrine therapy resistance occurs in a high proportion of patients with estrogen receptor alpha (ERα) and progesterone receptors (PR) positive breast cancer. We and others have previously shown that estrogen- and progestin-induced tumor growth requires ERα and PR interaction at their target genes. Here, we show that fibroblast growth factor 2 (FGF2)-induces cell proliferation and tumor growth through hormone-independent ERα and PR activation and their interaction at the MYC enhancer and proximal promoter. MYC inhibitors, antiestrogens or antiprogestins reverted FGF2-induced effects. LC?MS/MS identified 700 canonical proteins recruited to MYC regulatory sequences after FGF2 stimulation, 397 of which required active ERα (ERα-dependent). We identified ERα-dependent proteins regulating transcription that, after FGF2 treatment, were recruited to the enhancer as well as proteins involved in transcription initiation that were recruited to the proximal promoter. Also, among the ERα-dependent and independent proteins detected at both sites, PR isoforms A and B as well as the novel protein product PRBΔ4 were found. PRBΔ4 lacks the hormone-binding domain and was able to induce reporter gene expression from estrogen-regulated elements and to increase cell proliferation when cells were stimulated with FGF2 but not by progestins. Analysis of the Cancer Genome Atlas data set revealed that PRBΔ4 expression is associated with worse overall survival in luminal breast cancer patients. This discovery provides a new mechanism by which growth factor signaling can engage nonclassical hormone receptor isoforms such as PRBΔ4, which interacts with growth-factor activated ERα and PR to stimulate MYC gene expression and hence progression to endocrine resistance. Fil: Giulianelli, Sebastian Jesus. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Centro Nacional Patagónico. Instituto de Biología de Organismos Marinos; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Riggio, Marina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Guillardoy, Tomás. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Pérez Piñero, Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Gorostiaga, María A.. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Sequeira, Gonzalo Ricardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Pataccini, Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Abascal, María F.. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Toledo, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Jacobsen, Britta M.. University of Colorado; Estados Unidos Fil: Guerreiro, Ana C.. Universidade de Aveiro; Portugal Fil: Barros, António. Universidade de Aveiro; Portugal Fil: Novaro, Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Monteiro, Fátima L.. Universidade de Aveiro; Portugal Fil: Amado, Francisco. Universidade de Aveiro; Portugal Fil: Gass, Hugo. Hospital Zonal General de Agudos Magdalena V de Martínez; Argentina Fil: Abba, Martin. Universidad Nacional de La Plata; Argentina Fil: Helguero, Luisa A.. Universidade de Aveiro; Portugal Fil: Lanari, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina |
| description |
Progression to hormone-independent growth leading to endocrine therapy resistance occurs in a high proportion of patients with estrogen receptor alpha (ERα) and progesterone receptors (PR) positive breast cancer. We and others have previously shown that estrogen- and progestin-induced tumor growth requires ERα and PR interaction at their target genes. Here, we show that fibroblast growth factor 2 (FGF2)-induces cell proliferation and tumor growth through hormone-independent ERα and PR activation and their interaction at the MYC enhancer and proximal promoter. MYC inhibitors, antiestrogens or antiprogestins reverted FGF2-induced effects. LC?MS/MS identified 700 canonical proteins recruited to MYC regulatory sequences after FGF2 stimulation, 397 of which required active ERα (ERα-dependent). We identified ERα-dependent proteins regulating transcription that, after FGF2 treatment, were recruited to the enhancer as well as proteins involved in transcription initiation that were recruited to the proximal promoter. Also, among the ERα-dependent and independent proteins detected at both sites, PR isoforms A and B as well as the novel protein product PRBΔ4 were found. PRBΔ4 lacks the hormone-binding domain and was able to induce reporter gene expression from estrogen-regulated elements and to increase cell proliferation when cells were stimulated with FGF2 but not by progestins. Analysis of the Cancer Genome Atlas data set revealed that PRBΔ4 expression is associated with worse overall survival in luminal breast cancer patients. This discovery provides a new mechanism by which growth factor signaling can engage nonclassical hormone receptor isoforms such as PRBΔ4, which interacts with growth-factor activated ERα and PR to stimulate MYC gene expression and hence progression to endocrine resistance. |
| publishDate |
2019 |
| dc.date.none.fl_str_mv |
2019-03 |
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info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
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article |
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publishedVersion |
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http://hdl.handle.net/11336/107597 Giulianelli, Sebastian Jesus; Riggio, Marina; Guillardoy, Tomás; Pérez Piñero, Cecilia; Gorostiaga, María A.; et al.; FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences; John Wiley & Sons Inc; International Journal of Cancer; 145; 7; 3-2019; 1874-1888 0020-7136 1097-0215 CONICET Digital CONICET |
| url |
http://hdl.handle.net/11336/107597 |
| identifier_str_mv |
Giulianelli, Sebastian Jesus; Riggio, Marina; Guillardoy, Tomás; Pérez Piñero, Cecilia; Gorostiaga, María A.; et al.; FGF2 Induces Breast Cancer Growth through Ligand-Independent Activation and Recruitment of ERα and PRB∆4 Isoform to MYC Regulatory Sequences; John Wiley & Sons Inc; International Journal of Cancer; 145; 7; 3-2019; 1874-1888 0020-7136 1097-0215 CONICET Digital CONICET |
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eng |
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eng |
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John Wiley & Sons Inc |
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John Wiley & Sons Inc |
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