Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer

Autores
Menendez, Javier A.; Peirce, Susan K.; Papadimitropoulou, Adriana; Cuyàs, Elisabet; Steen, Travis Vander; Verdura, Sara; Vellón, Luciano; Chen, Wen Y.; Lupu, Ruth
Año de publicación
2020
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Progesterone receptor (PR) isoforms can drive unique phenotypes in luminal breast cancer (BC). Here, we hypothesized that PR-B and PR-A isoforms differentially modify the cross-talk between prolactin and fatty acid synthase (FASN) in BC. We profiled the responsiveness of the FASN gene promoter to prolactin in T47Dco BC cells constitutively expressing PR-A and PR-B, in the PR-null variant T47D-Y cell line, and in PR-null T47D-Y cells engineered to stably re-express PR-A (T47D-YA) or PR-B (T47D-YB). The capacity of prolactin to up-regulate FASN gene promoter activity in T47Dco cells was lost in T47D-Y and TD47-YA cells. Constitutively up-regulated FASN gene expression in T47-YB cells and its further stimulation by prolactin were both suppressed by the prolactin receptor antagonist hPRL-G129R. The ability of the FASN inhibitor C75 to decrease prolactin secretion was more conspicuous in T47-YB cells. In T47D-Y cells, which secreted notably less prolactin and downregulated prolactin receptor expression relative to T47Dco cells, FASN blockade resulted in an augmented secretion of prolactin and up-regulation of prolactin receptor expression. Our data reveal unforeseen PR-B isoform-specific regulatory actions in the cross-talk between prolactin and FASN signaling in BC. These findings might provide new PR-B/FASN-centered predictive and therapeutic modalities in luminal intrinsic BC subtypes
Fil: Menendez, Javier A.. Institut Català d'Oncologia; España. Institut d’Investigació Biomèdica de Girona; España
Fil: Peirce, Susan K.. Clemson University. Pearce Center Professional Communication; Estados Unidos
Fil: Papadimitropoulou, Adriana. Biomedical Research Foundation Academy of Athens; Grecia
Fil: Cuyàs, Elisabet. Institut Català d'Oncologia; España. Institut d’Investigació Biomèdica de Girona; España
Fil: Steen, Travis Vander. Mayo Foundation for Medical Education and Research. Mayo Clinic; Estados Unidos
Fil: Verdura, Sara. Institut Català d'Oncologia; España. Institut d’Investigació Biomèdica de Girona; España
Fil: Vellón, Luciano. 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: Chen, Wen Y.. Clemson University; Estados Unidos
Fil: Lupu, Ruth. Mayo Foundation for Medical Education and Research. Mayo Clinic; Estados Unidos. Clemson University; Estados Unidos. Mayo Clinic Cancer Center; Estados Unidos
Materia
ENDOCRINE THERAPY
G129R
LUMINAL BREAST CANCER
PROLACTIN RECEPTOR
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:11336/131957

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repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancerMenendez, Javier A.Peirce, Susan K.Papadimitropoulou, AdrianaCuyàs, ElisabetSteen, Travis VanderVerdura, SaraVellón, LucianoChen, Wen Y.Lupu, RuthENDOCRINE THERAPYG129RLUMINAL BREAST CANCERPROLACTIN RECEPTORhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Progesterone receptor (PR) isoforms can drive unique phenotypes in luminal breast cancer (BC). Here, we hypothesized that PR-B and PR-A isoforms differentially modify the cross-talk between prolactin and fatty acid synthase (FASN) in BC. We profiled the responsiveness of the FASN gene promoter to prolactin in T47Dco BC cells constitutively expressing PR-A and PR-B, in the PR-null variant T47D-Y cell line, and in PR-null T47D-Y cells engineered to stably re-express PR-A (T47D-YA) or PR-B (T47D-YB). The capacity of prolactin to up-regulate FASN gene promoter activity in T47Dco cells was lost in T47D-Y and TD47-YA cells. Constitutively up-regulated FASN gene expression in T47-YB cells and its further stimulation by prolactin were both suppressed by the prolactin receptor antagonist hPRL-G129R. The ability of the FASN inhibitor C75 to decrease prolactin secretion was more conspicuous in T47-YB cells. In T47D-Y cells, which secreted notably less prolactin and downregulated prolactin receptor expression relative to T47Dco cells, FASN blockade resulted in an augmented secretion of prolactin and up-regulation of prolactin receptor expression. Our data reveal unforeseen PR-B isoform-specific regulatory actions in the cross-talk between prolactin and FASN signaling in BC. These findings might provide new PR-B/FASN-centered predictive and therapeutic modalities in luminal intrinsic BC subtypesFil: Menendez, Javier A.. Institut Català d'Oncologia; España. Institut d’Investigació Biomèdica de Girona; EspañaFil: Peirce, Susan K.. Clemson University. Pearce Center Professional Communication; Estados UnidosFil: Papadimitropoulou, Adriana. Biomedical Research Foundation Academy of Athens; GreciaFil: Cuyàs, Elisabet. Institut Català d'Oncologia; España. Institut d’Investigació Biomèdica de Girona; EspañaFil: Steen, Travis Vander. Mayo Foundation for Medical Education and Research. Mayo Clinic; Estados UnidosFil: Verdura, Sara. Institut Català d'Oncologia; España. Institut d’Investigació Biomèdica de Girona; EspañaFil: Vellón, Luciano. 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: Chen, Wen Y.. Clemson University; Estados UnidosFil: Lupu, Ruth. Mayo Foundation for Medical Education and Research. Mayo Clinic; Estados Unidos. Clemson University; Estados Unidos. Mayo Clinic Cancer Center; Estados UnidosImpact Journals2020-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/131957Menendez, Javier A.; Peirce, Susan K.; Papadimitropoulou, Adriana; Cuyàs, Elisabet; Steen, Travis Vander; et al.; Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer; Impact Journals; Aging; 12; 24; 12-2020; 24671-246921945-4589CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.18632/aging.202289info:eu-repo/semantics/altIdentifier/url/https://www.aging-us.com/article/202289/textinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:33:38Zoai:ri.conicet.gov.ar:11336/131957instacron: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:34982025-09-29 10:33:38.733CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer
title Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer
spellingShingle Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer
Menendez, Javier A.
ENDOCRINE THERAPY
G129R
LUMINAL BREAST CANCER
PROLACTIN RECEPTOR
title_short Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer
title_full Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer
title_fullStr Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer
title_full_unstemmed Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer
title_sort Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer
dc.creator.none.fl_str_mv Menendez, Javier A.
Peirce, Susan K.
Papadimitropoulou, Adriana
Cuyàs, Elisabet
Steen, Travis Vander
Verdura, Sara
Vellón, Luciano
Chen, Wen Y.
Lupu, Ruth
author Menendez, Javier A.
author_facet Menendez, Javier A.
Peirce, Susan K.
Papadimitropoulou, Adriana
Cuyàs, Elisabet
Steen, Travis Vander
Verdura, Sara
Vellón, Luciano
Chen, Wen Y.
Lupu, Ruth
author_role author
author2 Peirce, Susan K.
Papadimitropoulou, Adriana
Cuyàs, Elisabet
Steen, Travis Vander
Verdura, Sara
Vellón, Luciano
Chen, Wen Y.
Lupu, Ruth
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv ENDOCRINE THERAPY
G129R
LUMINAL BREAST CANCER
PROLACTIN RECEPTOR
topic ENDOCRINE THERAPY
G129R
LUMINAL BREAST CANCER
PROLACTIN RECEPTOR
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Progesterone receptor (PR) isoforms can drive unique phenotypes in luminal breast cancer (BC). Here, we hypothesized that PR-B and PR-A isoforms differentially modify the cross-talk between prolactin and fatty acid synthase (FASN) in BC. We profiled the responsiveness of the FASN gene promoter to prolactin in T47Dco BC cells constitutively expressing PR-A and PR-B, in the PR-null variant T47D-Y cell line, and in PR-null T47D-Y cells engineered to stably re-express PR-A (T47D-YA) or PR-B (T47D-YB). The capacity of prolactin to up-regulate FASN gene promoter activity in T47Dco cells was lost in T47D-Y and TD47-YA cells. Constitutively up-regulated FASN gene expression in T47-YB cells and its further stimulation by prolactin were both suppressed by the prolactin receptor antagonist hPRL-G129R. The ability of the FASN inhibitor C75 to decrease prolactin secretion was more conspicuous in T47-YB cells. In T47D-Y cells, which secreted notably less prolactin and downregulated prolactin receptor expression relative to T47Dco cells, FASN blockade resulted in an augmented secretion of prolactin and up-regulation of prolactin receptor expression. Our data reveal unforeseen PR-B isoform-specific regulatory actions in the cross-talk between prolactin and FASN signaling in BC. These findings might provide new PR-B/FASN-centered predictive and therapeutic modalities in luminal intrinsic BC subtypes
Fil: Menendez, Javier A.. Institut Català d'Oncologia; España. Institut d’Investigació Biomèdica de Girona; España
Fil: Peirce, Susan K.. Clemson University. Pearce Center Professional Communication; Estados Unidos
Fil: Papadimitropoulou, Adriana. Biomedical Research Foundation Academy of Athens; Grecia
Fil: Cuyàs, Elisabet. Institut Català d'Oncologia; España. Institut d’Investigació Biomèdica de Girona; España
Fil: Steen, Travis Vander. Mayo Foundation for Medical Education and Research. Mayo Clinic; Estados Unidos
Fil: Verdura, Sara. Institut Català d'Oncologia; España. Institut d’Investigació Biomèdica de Girona; España
Fil: Vellón, Luciano. 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: Chen, Wen Y.. Clemson University; Estados Unidos
Fil: Lupu, Ruth. Mayo Foundation for Medical Education and Research. Mayo Clinic; Estados Unidos. Clemson University; Estados Unidos. Mayo Clinic Cancer Center; Estados Unidos
description Progesterone receptor (PR) isoforms can drive unique phenotypes in luminal breast cancer (BC). Here, we hypothesized that PR-B and PR-A isoforms differentially modify the cross-talk between prolactin and fatty acid synthase (FASN) in BC. We profiled the responsiveness of the FASN gene promoter to prolactin in T47Dco BC cells constitutively expressing PR-A and PR-B, in the PR-null variant T47D-Y cell line, and in PR-null T47D-Y cells engineered to stably re-express PR-A (T47D-YA) or PR-B (T47D-YB). The capacity of prolactin to up-regulate FASN gene promoter activity in T47Dco cells was lost in T47D-Y and TD47-YA cells. Constitutively up-regulated FASN gene expression in T47-YB cells and its further stimulation by prolactin were both suppressed by the prolactin receptor antagonist hPRL-G129R. The ability of the FASN inhibitor C75 to decrease prolactin secretion was more conspicuous in T47-YB cells. In T47D-Y cells, which secreted notably less prolactin and downregulated prolactin receptor expression relative to T47Dco cells, FASN blockade resulted in an augmented secretion of prolactin and up-regulation of prolactin receptor expression. Our data reveal unforeseen PR-B isoform-specific regulatory actions in the cross-talk between prolactin and FASN signaling in BC. These findings might provide new PR-B/FASN-centered predictive and therapeutic modalities in luminal intrinsic BC subtypes
publishDate 2020
dc.date.none.fl_str_mv 2020-12
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/11336/131957
Menendez, Javier A.; Peirce, Susan K.; Papadimitropoulou, Adriana; Cuyàs, Elisabet; Steen, Travis Vander; et al.; Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer; Impact Journals; Aging; 12; 24; 12-2020; 24671-24692
1945-4589
CONICET Digital
CONICET
url http://hdl.handle.net/11336/131957
identifier_str_mv Menendez, Javier A.; Peirce, Susan K.; Papadimitropoulou, Adriana; Cuyàs, Elisabet; Steen, Travis Vander; et al.; Progesterone receptor isoform-dependent cross-talk between prolactin and fatty acid synthase in breast cancer; Impact Journals; Aging; 12; 24; 12-2020; 24671-24692
1945-4589
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.18632/aging.202289
info:eu-repo/semantics/altIdentifier/url/https://www.aging-us.com/article/202289/text
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
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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