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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/47949
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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 Técnicas2025-09-29T09:33:42Zoai: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:34982025-09-29 09:33:43.202CONICET 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 |
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1844613037768572928 |
score |
13.070432 |