RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts

Autores
Rodríguez, Maria Sol; Riggio, Marina; Lamb, Caroline Ana; Vanzulli, Silvia; Luthy, Isabel Alicia; Lanari, Claudia Lee Malvina; Pérez Piñero, Cecilia
Año de publicación
2021
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
T47D and IBH6 cells that overexpress RUNX2 show high levels of FGFR2 and FGF2, supporting the hypothesis that FGF2 increases RUNX2 and, in turn, RUNX2 increases FGF2, maintaining a positive loop. However, in these models RUNX2 overexpression generates tumors resistant to FGFR inhibitor therapy and show a more aggressive phenotype compared with control tumors.T47D and IBH6 are luminal breast cancer cells that express ER and PR. Our goal is to explore the role of RUNX2 and its relationship with hormone receptors in BrCa. The aim of this work was to evaluate the effect of endocrine therapy in RUNX2 overexpressing tumors.RUNX2 and control cells (C, empty vector) were injected into the flank of NSG mice. Animals were treated for 3 weeks with an antiestrogen (Fulvestrant FUL, 0.5mg/week) or an antiprogestin (MFP, 6mg pellets). Control tumors showed a significant growth inhibition with the therapy (C-T47D p<0.0001 C vs FUL and MFP; C-IBH6 p<0.0001 C vs FUL), a lower Ki67 index (C-T47D: p<0.0001 C vs FUL, p<0.05 C vs MFP, C-IBH6 p<0.05 C vs FUL) and higher stromal remodeling compared with untreated ones. In both models, RUNX2 tumors were resistant to endocrine therapy and all animals bearing RUNX2-T47D tumors developed lung metastasis. Our conclusion is that RUNX2 promotes BrCa progression and is a key player in the acquisition of endocrine resistance. We emphasize the development of RUNX2 inhibitors to use in combination with standard therapy for BrCa treatment.
Fil: Rodríguez, Maria Sol. 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: Lamb, Caroline Ana. 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: Vanzulli, Silvia. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Luthy, Isabel Alicia. 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: Lanari, Claudia Lee Malvina. 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
Buenos Aires Breast Cancer Symposium
Buenos Aires
Argentina
Centro de Educación Médica e Investigaciones Clínicas “Norberto Quirno”
Consejo Nacional de Investigaciones Científicas y Técnicas
Instituto de Biología y Medicina Experimental
Instituto de Fisiología, Biología Molecular y Neurociencias
Instituto de Investigaciones en Medicina Traslacional
Instituto de Nanosistemas
Universidad Austral
Universidad de Buenos Aires
Universidad Nacional de San Martín
Materia
RUNX-2
BREAST CANCER
LUMINAL TUMOR
ENDOCRINE RESISTANCE
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:11336/152261
Acceder
id CONICETDig_65baf9a081e8164f09161b182b45e2cf
oai_identifier_str oai:ri.conicet.gov.ar:11336/152261
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenograftsRodríguez, Maria SolRiggio, MarinaLamb, Caroline AnaVanzulli, SilviaLuthy, Isabel AliciaLanari, Claudia Lee MalvinaPérez Piñero, CeciliaRUNX-2BREAST CANCERLUMINAL TUMORENDOCRINE RESISTANCEhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3https://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3T47D and IBH6 cells that overexpress RUNX2 show high levels of FGFR2 and FGF2, supporting the hypothesis that FGF2 increases RUNX2 and, in turn, RUNX2 increases FGF2, maintaining a positive loop. However, in these models RUNX2 overexpression generates tumors resistant to FGFR inhibitor therapy and show a more aggressive phenotype compared with control tumors.T47D and IBH6 are luminal breast cancer cells that express ER and PR. Our goal is to explore the role of RUNX2 and its relationship with hormone receptors in BrCa. The aim of this work was to evaluate the effect of endocrine therapy in RUNX2 overexpressing tumors.RUNX2 and control cells (C, empty vector) were injected into the flank of NSG mice. Animals were treated for 3 weeks with an antiestrogen (Fulvestrant FUL, 0.5mg/week) or an antiprogestin (MFP, 6mg pellets). Control tumors showed a significant growth inhibition with the therapy (C-T47D p<0.0001 C vs FUL and MFP; C-IBH6 p<0.0001 C vs FUL), a lower Ki67 index (C-T47D: p<0.0001 C vs FUL, p<0.05 C vs MFP, C-IBH6 p<0.05 C vs FUL) and higher stromal remodeling compared with untreated ones. In both models, RUNX2 tumors were resistant to endocrine therapy and all animals bearing RUNX2-T47D tumors developed lung metastasis. Our conclusion is that RUNX2 promotes BrCa progression and is a key player in the acquisition of endocrine resistance. We emphasize the development of RUNX2 inhibitors to use in combination with standard therapy for BrCa treatment.Fil: Rodríguez, Maria Sol. 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: Lamb, Caroline Ana. 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: Vanzulli, Silvia. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Luthy, Isabel Alicia. 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: Lanari, Claudia Lee Malvina. 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; ArgentinaBuenos Aires Breast Cancer SymposiumBuenos AiresArgentinaCentro de Educación Médica e Investigaciones Clínicas “Norberto Quirno”Consejo Nacional de Investigaciones Científicas y TécnicasInstituto de Biología y Medicina ExperimentalInstituto de Fisiología, Biología Molecular y NeurocienciasInstituto de Investigaciones en Medicina TraslacionalInstituto de NanosistemasUniversidad AustralUniversidad de Buenos AiresUniversidad Nacional de San MartínFundación Revista MedicinaKordon, Edith ClaudiaLanari, Claudia Lee MalvinaSimian, Marina2021info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectSimposioJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/152261RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts; Buenos Aires Breast Cancer Symposium; Buenos Aires; Argentina; 2021; 25-250025-76801669-9106CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://ba-bcs2020.com/info:eu-repo/semantics/altIdentifier/url/https://vcongress.ba-bcs2020.com/poster/runx2-overexpression-generates-endocrine-resistance-in-human-luminal-breast-cancer-xenografts/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 Técnicas2025-09-03T09:43:38Zoai:ri.conicet.gov.ar:11336/152261instacron: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 09:43:38.632CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts
title RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts
spellingShingle RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts
Rodríguez, Maria Sol
RUNX-2
BREAST CANCER
LUMINAL TUMOR
ENDOCRINE RESISTANCE
title_short RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts
title_full RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts
title_fullStr RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts
title_full_unstemmed RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts
title_sort RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts
dc.creator.none.fl_str_mv Rodríguez, Maria Sol
Riggio, Marina
Lamb, Caroline Ana
Vanzulli, Silvia
Luthy, Isabel Alicia
Lanari, Claudia Lee Malvina
Pérez Piñero, Cecilia
author Rodríguez, Maria Sol
author_facet Rodríguez, Maria Sol
Riggio, Marina
Lamb, Caroline Ana
Vanzulli, Silvia
Luthy, Isabel Alicia
Lanari, Claudia Lee Malvina
Pérez Piñero, Cecilia
author_role author
author2 Riggio, Marina
Lamb, Caroline Ana
Vanzulli, Silvia
Luthy, Isabel Alicia
Lanari, Claudia Lee Malvina
Pérez Piñero, Cecilia
author2_role author
author
author
author
author
author
dc.contributor.none.fl_str_mv Kordon, Edith Claudia
Lanari, Claudia Lee Malvina
Simian, Marina
dc.subject.none.fl_str_mv RUNX-2
BREAST CANCER
LUMINAL TUMOR
ENDOCRINE RESISTANCE
topic RUNX-2
BREAST CANCER
LUMINAL TUMOR
ENDOCRINE RESISTANCE
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv T47D and IBH6 cells that overexpress RUNX2 show high levels of FGFR2 and FGF2, supporting the hypothesis that FGF2 increases RUNX2 and, in turn, RUNX2 increases FGF2, maintaining a positive loop. However, in these models RUNX2 overexpression generates tumors resistant to FGFR inhibitor therapy and show a more aggressive phenotype compared with control tumors.T47D and IBH6 are luminal breast cancer cells that express ER and PR. Our goal is to explore the role of RUNX2 and its relationship with hormone receptors in BrCa. The aim of this work was to evaluate the effect of endocrine therapy in RUNX2 overexpressing tumors.RUNX2 and control cells (C, empty vector) were injected into the flank of NSG mice. Animals were treated for 3 weeks with an antiestrogen (Fulvestrant FUL, 0.5mg/week) or an antiprogestin (MFP, 6mg pellets). Control tumors showed a significant growth inhibition with the therapy (C-T47D p<0.0001 C vs FUL and MFP; C-IBH6 p<0.0001 C vs FUL), a lower Ki67 index (C-T47D: p<0.0001 C vs FUL, p<0.05 C vs MFP, C-IBH6 p<0.05 C vs FUL) and higher stromal remodeling compared with untreated ones. In both models, RUNX2 tumors were resistant to endocrine therapy and all animals bearing RUNX2-T47D tumors developed lung metastasis. Our conclusion is that RUNX2 promotes BrCa progression and is a key player in the acquisition of endocrine resistance. We emphasize the development of RUNX2 inhibitors to use in combination with standard therapy for BrCa treatment.
Fil: Rodríguez, Maria Sol. 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: Lamb, Caroline Ana. 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: Vanzulli, Silvia. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Luthy, Isabel Alicia. 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: Lanari, Claudia Lee Malvina. 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
Buenos Aires Breast Cancer Symposium
Buenos Aires
Argentina
Centro de Educación Médica e Investigaciones Clínicas “Norberto Quirno”
Consejo Nacional de Investigaciones Científicas y Técnicas
Instituto de Biología y Medicina Experimental
Instituto de Fisiología, Biología Molecular y Neurociencias
Instituto de Investigaciones en Medicina Traslacional
Instituto de Nanosistemas
Universidad Austral
Universidad de Buenos Aires
Universidad Nacional de San Martín
description T47D and IBH6 cells that overexpress RUNX2 show high levels of FGFR2 and FGF2, supporting the hypothesis that FGF2 increases RUNX2 and, in turn, RUNX2 increases FGF2, maintaining a positive loop. However, in these models RUNX2 overexpression generates tumors resistant to FGFR inhibitor therapy and show a more aggressive phenotype compared with control tumors.T47D and IBH6 are luminal breast cancer cells that express ER and PR. Our goal is to explore the role of RUNX2 and its relationship with hormone receptors in BrCa. The aim of this work was to evaluate the effect of endocrine therapy in RUNX2 overexpressing tumors.RUNX2 and control cells (C, empty vector) were injected into the flank of NSG mice. Animals were treated for 3 weeks with an antiestrogen (Fulvestrant FUL, 0.5mg/week) or an antiprogestin (MFP, 6mg pellets). Control tumors showed a significant growth inhibition with the therapy (C-T47D p<0.0001 C vs FUL and MFP; C-IBH6 p<0.0001 C vs FUL), a lower Ki67 index (C-T47D: p<0.0001 C vs FUL, p<0.05 C vs MFP, C-IBH6 p<0.05 C vs FUL) and higher stromal remodeling compared with untreated ones. In both models, RUNX2 tumors were resistant to endocrine therapy and all animals bearing RUNX2-T47D tumors developed lung metastasis. Our conclusion is that RUNX2 promotes BrCa progression and is a key player in the acquisition of endocrine resistance. We emphasize the development of RUNX2 inhibitors to use in combination with standard therapy for BrCa treatment.
publishDate 2021
dc.date.none.fl_str_mv 2021
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Simposio
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/11336/152261
RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts; Buenos Aires Breast Cancer Symposium; Buenos Aires; Argentina; 2021; 25-25
0025-7680
1669-9106
CONICET Digital
CONICET
url http://hdl.handle.net/11336/152261
identifier_str_mv RUNX2 overexpression generates endocrine resistance in human luminal breast cancer xenografts; Buenos Aires Breast Cancer Symposium; Buenos Aires; Argentina; 2021; 25-25
0025-7680
1669-9106
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://ba-bcs2020.com/
info:eu-repo/semantics/altIdentifier/url/https://vcongress.ba-bcs2020.com/poster/runx2-overexpression-generates-endocrine-resistance-in-human-luminal-breast-cancer-xenografts/
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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