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dc.contributor.author Todaro, Laura Beatriz
dc.contributor.author Veloso, María José
dc.contributor.author Campodónico, Paola Bernadette
dc.contributor.author Puricelli, Lydia Ines
dc.contributor.author Farias, Eduardo Francisco
dc.contributor.author Bal, Elisa Dora
dc.date.available 2017-03-21T20:16:02Z
dc.date.issued 2013-10
dc.identifier.citation Todaro, Laura Beatriz; Veloso, María José; Campodónico, Paola Bernadette; Puricelli, Lydia Ines; Farias, Eduardo Francisco; et al.; A clinically relevant bi-cellular murine mammary tumor model as a useful tool for evaluating the effect of retinoic acid signaling on tumor progression; Springer Tokyo; Breast Cancer; 20; 4; 10-2013; 342-356
dc.identifier.issn 1340-6868
dc.identifier.uri http://hdl.handle.net/11336/14139
dc.description.abstract BACKGROUND: The effect of retinoic acid (RA) on breast cancer progression is controversial. Our objective was to obtain information about breast cancer progression, taking advantage of the ER-negative murine mammary adenocarcinoma model LM38 (LM38-LP constituted by luminal (LEP) and myoepithelial-like cells (MEP), LM38-HP mainly composed of spindle-shaped epithelial cells, and LM38-D2 containing only large myoepithelial cells), and to validate the role of the retinoic acid receptors (RARs) in each cell-type compartment. MATERIALS AND METHODS: We studied the expression and functionality of the RARs in LM38 cell lines. We analyzed cell growth and cell cycle distribution, apoptosis, the activity of proteases, motility properties, and expression of the molecules involved in these pathways. We also evaluated tumor growth and dissemination in vivo under retinoid treatment. RESULTS: LM38 cell lines expressed most retinoic receptor isotypes that were functional. However, only the bi-cellular LM38-LP cells responded to retinoids by increasing RARβ2 and CRBP1 expression. The growth of LM38 cell sublines was inhibited by retinoids, first by inducing arrest in MEP cells, then apoptosis in LEP cells. Retinoids induced inhibitory effects on motility, invasiveness, and activity of proteolytic enzymes, mainly in the LM38-LP cell line. In in-vivo assays with the LM38-LP cell line, RA treatment impaired both primary tumor growth and lung metastases dissemination. CCONCLUSION: These in-vivo and in-vitro results show that to achieve maximum effects of RA on tumor progression both the LEP and MEP cell compartments have to be present, suggesting that the interaction between the LEP and MEP cells is crucial to full activation of the RARs.
dc.format application/pdf
dc.language.iso eng
dc.publisher Springer Tokyo
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject BREAST CANCER
dc.subject LUMINAL AND MYOEPITHELIAL CELLS
dc.subject RETINOIDS
dc.subject METASTASIS
dc.subject.classification Otras Ciencias de la Salud
dc.subject.classification Ciencias de la Salud
dc.subject.classification CIENCIAS MÉDICAS Y DE LA SALUD
dc.title A clinically relevant bi-cellular murine mammary tumor model as a useful tool for evaluating the effect of retinoic acid signaling on tumor progression
dc.type info:eu-repo/semantics/article
dc.type info:ar-repo/semantics/artículo
dc.type info:eu-repo/semantics/publishedVersion
dc.date.updated 2017-03-20T17:41:21Z
dc.identifier.eissn 1880-4233
dc.journal.volume 20
dc.journal.number 4
dc.journal.pagination 342-356
dc.journal.pais Japón
dc.journal.ciudad Tokio
dc.description.fil Fil: Todaro, Laura Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina
dc.description.fil Fil: Veloso, María José. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina
dc.description.fil Fil: Campodónico, Paola Bernadette. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina
dc.description.fil Fil: Puricelli, Lydia Ines. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina
dc.description.fil Fil: Farias, Eduardo Francisco. Mount Sinai School of Medicine; Estados Unidos
dc.description.fil Fil: Bal, Elisa Dora. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina
dc.journal.title Breast Cancer
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/url/http://rd.springer.com/article/10.1007/s12282-012-0342-5#
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s12282-012-0342-5


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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)