Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway

Autores
Berardi, Damian Emilio; Raffo, Diego Alejandro; Todaro, Laura Beatriz; Simian, Marina
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
PURPOSE: We investigated the effects of laminin on the fraction of cells with self-renewing capacity in the estrogen-dependent, tamoxifen-sensitive LM05-E breast cancer cell line. We also determined whether laminin affected the response to tamoxifen. MATERIALS AND METHODS: The LM05-E breast cancer cell line was used as a model for all experiments. Aldehyde dehydrogenase (ALDH) activity, clonogenic and mammosphere assays were performed to measure the effects of laminin on modulation of the stem cell subpopulation. Pluripotent gene expression was analyzed by RT-PCR. The involvement of the MAPK/ERK pathway was determined using specific inhibitors. The effects of laminin on the response to tamoxifen were determined and the involvement of alpha-6 integrin was investigated. RESULTS: We found that pre-treatment with laminin leads to a decrease in cells with the ability to form mammospheres that was accompanied by a decrease in ALDH activity. Moreover, exposure of mammospheres to laminin reduced the capacity to form secondary mammospheres and decreased the expression of Sox-2, Nanog and Oct-4. We previously reported that 4-OH-tamoxifen leads to an increase in the expression of these genes in LM05-E cells. Treatment with signaling pathway inhibitors revealed that the MAPK/ERK pathway mediates the effects of laminin. Finally, laminin induced tamoxifen resistance in LM05-E cells through alpha 6 integrin. CONCLUSIONS: Our results suggest that the final number of cells with self-renewing capacity in estrogen-dependent breast tumors may result from the combined effects of endocrine treatment and microenvironmental cues.
Fil: Berardi, Damian Emilio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentina
Fil: Raffo, Diego Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentina
Fil: Todaro, Laura Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentina
Fil: Simian, Marina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martin. Instituto de Nanosistemas; Argentina
Materia
LAMININ
BREAST NEOPLASMS
ESTROGEN RECEPTOR ALPHA
STEM CELLS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/47949
Acceder
id CONICETDig_da319cdcc8017a6baf53b3c8e7667b96
oai_identifier_str oai:ri.conicet.gov.ar:11336/47949
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK PathwayBerardi, Damian EmilioRaffo, Diego AlejandroTodaro, Laura BeatrizSimian, MarinaLAMININBREAST NEOPLASMSESTROGEN RECEPTOR ALPHASTEM CELLShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3PURPOSE: We investigated the effects of laminin on the fraction of cells with self-renewing capacity in the estrogen-dependent, tamoxifen-sensitive LM05-E breast cancer cell line. We also determined whether laminin affected the response to tamoxifen. MATERIALS AND METHODS: The LM05-E breast cancer cell line was used as a model for all experiments. Aldehyde dehydrogenase (ALDH) activity, clonogenic and mammosphere assays were performed to measure the effects of laminin on modulation of the stem cell subpopulation. Pluripotent gene expression was analyzed by RT-PCR. The involvement of the MAPK/ERK pathway was determined using specific inhibitors. The effects of laminin on the response to tamoxifen were determined and the involvement of alpha-6 integrin was investigated. RESULTS: We found that pre-treatment with laminin leads to a decrease in cells with the ability to form mammospheres that was accompanied by a decrease in ALDH activity. Moreover, exposure of mammospheres to laminin reduced the capacity to form secondary mammospheres and decreased the expression of Sox-2, Nanog and Oct-4. We previously reported that 4-OH-tamoxifen leads to an increase in the expression of these genes in LM05-E cells. Treatment with signaling pathway inhibitors revealed that the MAPK/ERK pathway mediates the effects of laminin. Finally, laminin induced tamoxifen resistance in LM05-E cells through alpha 6 integrin. CONCLUSIONS: Our results suggest that the final number of cells with self-renewing capacity in estrogen-dependent breast tumors may result from the combined effects of endocrine treatment and microenvironmental cues.Fil: Berardi, Damian Emilio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; ArgentinaFil: Raffo, Diego Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; ArgentinaFil: Todaro, Laura Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; ArgentinaFil: Simian, Marina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martin. Instituto de Nanosistemas; ArgentinaKorean Cancer Association2016-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/47949Berardi, Damian Emilio; Raffo, Diego Alejandro; Todaro, Laura Beatriz; Simian, Marina; Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway; Korean Cancer Association; Cancer Research and Treatment; 49; 4; 12-2016; 869-8791598-29982005-9256CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.4143/crt.2016.378info:eu-repo/semantics/altIdentifier/url/https://www.e-crt.org/journal/view.php?doi=10.4143/crt.2016.378info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5654159/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T14:21:51Zoai:ri.conicet.gov.ar:11336/47949instacron: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:34982025-10-15 14:21:52.082CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway
title Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway
spellingShingle Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway
Berardi, Damian Emilio
LAMININ
BREAST NEOPLASMS
ESTROGEN RECEPTOR ALPHA
STEM CELLS
title_short Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway
title_full Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway
title_fullStr Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway
title_full_unstemmed Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway
title_sort Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway
dc.creator.none.fl_str_mv Berardi, Damian Emilio
Raffo, Diego Alejandro
Todaro, Laura Beatriz
Simian, Marina
author Berardi, Damian Emilio
author_facet Berardi, Damian Emilio
Raffo, Diego Alejandro
Todaro, Laura Beatriz
Simian, Marina
author_role author
author2 Raffo, Diego Alejandro
Todaro, Laura Beatriz
Simian, Marina
author2_role author
author
author
dc.subject.none.fl_str_mv LAMININ
BREAST NEOPLASMS
ESTROGEN RECEPTOR ALPHA
STEM CELLS
topic LAMININ
BREAST NEOPLASMS
ESTROGEN RECEPTOR ALPHA
STEM CELLS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv PURPOSE: We investigated the effects of laminin on the fraction of cells with self-renewing capacity in the estrogen-dependent, tamoxifen-sensitive LM05-E breast cancer cell line. We also determined whether laminin affected the response to tamoxifen. MATERIALS AND METHODS: The LM05-E breast cancer cell line was used as a model for all experiments. Aldehyde dehydrogenase (ALDH) activity, clonogenic and mammosphere assays were performed to measure the effects of laminin on modulation of the stem cell subpopulation. Pluripotent gene expression was analyzed by RT-PCR. The involvement of the MAPK/ERK pathway was determined using specific inhibitors. The effects of laminin on the response to tamoxifen were determined and the involvement of alpha-6 integrin was investigated. RESULTS: We found that pre-treatment with laminin leads to a decrease in cells with the ability to form mammospheres that was accompanied by a decrease in ALDH activity. Moreover, exposure of mammospheres to laminin reduced the capacity to form secondary mammospheres and decreased the expression of Sox-2, Nanog and Oct-4. We previously reported that 4-OH-tamoxifen leads to an increase in the expression of these genes in LM05-E cells. Treatment with signaling pathway inhibitors revealed that the MAPK/ERK pathway mediates the effects of laminin. Finally, laminin induced tamoxifen resistance in LM05-E cells through alpha 6 integrin. CONCLUSIONS: Our results suggest that the final number of cells with self-renewing capacity in estrogen-dependent breast tumors may result from the combined effects of endocrine treatment and microenvironmental cues.
Fil: Berardi, Damian Emilio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentina
Fil: Raffo, Diego Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentina
Fil: Todaro, Laura Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología ; Argentina
Fil: Simian, Marina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martin. Instituto de Nanosistemas; Argentina
description PURPOSE: We investigated the effects of laminin on the fraction of cells with self-renewing capacity in the estrogen-dependent, tamoxifen-sensitive LM05-E breast cancer cell line. We also determined whether laminin affected the response to tamoxifen. MATERIALS AND METHODS: The LM05-E breast cancer cell line was used as a model for all experiments. Aldehyde dehydrogenase (ALDH) activity, clonogenic and mammosphere assays were performed to measure the effects of laminin on modulation of the stem cell subpopulation. Pluripotent gene expression was analyzed by RT-PCR. The involvement of the MAPK/ERK pathway was determined using specific inhibitors. The effects of laminin on the response to tamoxifen were determined and the involvement of alpha-6 integrin was investigated. RESULTS: We found that pre-treatment with laminin leads to a decrease in cells with the ability to form mammospheres that was accompanied by a decrease in ALDH activity. Moreover, exposure of mammospheres to laminin reduced the capacity to form secondary mammospheres and decreased the expression of Sox-2, Nanog and Oct-4. We previously reported that 4-OH-tamoxifen leads to an increase in the expression of these genes in LM05-E cells. Treatment with signaling pathway inhibitors revealed that the MAPK/ERK pathway mediates the effects of laminin. Finally, laminin induced tamoxifen resistance in LM05-E cells through alpha 6 integrin. CONCLUSIONS: Our results suggest that the final number of cells with self-renewing capacity in estrogen-dependent breast tumors may result from the combined effects of endocrine treatment and microenvironmental cues.
publishDate 2016
dc.date.none.fl_str_mv 2016-12
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/11336/47949
Berardi, Damian Emilio; Raffo, Diego Alejandro; Todaro, Laura Beatriz; Simian, Marina; Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway; Korean Cancer Association; Cancer Research and Treatment; 49; 4; 12-2016; 869-879
1598-2998
2005-9256
CONICET Digital
CONICET
url http://hdl.handle.net/11336/47949
identifier_str_mv Berardi, Damian Emilio; Raffo, Diego Alejandro; Todaro, Laura Beatriz; Simian, Marina; Laminin Modulates the Stem Cell Population in LM05-E Murine Breast Cancer Cells Through the Activation of the MAPK/ERK Pathway; Korean Cancer Association; Cancer Research and Treatment; 49; 4; 12-2016; 869-879
1598-2998
2005-9256
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.4143/crt.2016.378
info:eu-repo/semantics/altIdentifier/url/https://www.e-crt.org/journal/view.php?doi=10.4143/crt.2016.378
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5654159/
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Korean Cancer Association
publisher.none.fl_str_mv Korean Cancer Association
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
_version_ 1846082610265063424
score 13.22299

Publicaciones similares