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Artículo

Downregulation of adaptor protein MyD88 compromises the angiogenic potential of B16 murine melanoma

Trucco, Lucas DanielIcon ; Roselli, EmilianoIcon ; Araya, PaulaIcon ; Nuñez, Nicolás Gonzalo; Mena, Hebe AgustinaIcon ; Bocco, Jose LuisIcon ; Negrotto, SoledadIcon ; Maccioni, MarianaIcon
Fecha de publicación: 06/2017
Editorial: Public Library of Science
Revista: Plos One
e-ISSN: 1932-6203
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Medicina Forense

Resumen

The mechanisms that link inflammatory responses to cancer development remain a subject of intense investigation, emphasizing the need to better understand the cellular and molecular pathways that create a tumor promoting microenvironment. The myeloid differentiation primary response protein MyD88 acts as a main adaptor molecule for the signaling cascades initiated from Toll-like receptors (TLRs) and the interleukin 1 receptor (IL-1R). MyD88 has been shown to contribute to tumorigenesis in many inflammation-associated cancer models. In this study, we sought to better define the role of MyD88 in neoplastic cells using a murine melanoma model. Herein, we have demonstrated that MyD88 expression is required to maintain the angiogenic switch that supports B16 melanoma growth. By knocking down MyD88 we reduced TLR-mediated NF-κB activation with no evident effects over cell proliferation and survival. In addition, MyD88 downregulation was associated with a decrease of HIF1α levels and its target gene VEGF, in correlation with an impaired capability to induce capillary sprouting and tube formation of endothelial cells. Melanomas developed from cells lacking MyD88 showed an enhanced secretion of chemoattractant ligands such as CCL2, CXCL10 and CXCL1 and have an improved infiltration of macrophages to the tumor site. Our results imply that cell-autonomous signaling through MyD88 is required to sustain tumor growth and underscore its function as an important positive modulator of tumor angiogenesis.
Palabras clave: Myd88 , Angiogenesis , Toll-Like Receptors
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution 2.5 Unported (CC BY 2.5)
Identificadores
URI: http://hdl.handle.net/11336/48488
DOI: https://dx.doi.org/10.1371/journal.pone.0179897
URL: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0179897
Colecciones
Articulos(CIBICI)
Articulos de CENTRO DE INV.EN BIOQUI.CLINICA E INMUNOLOGIA
Articulos(IMEX)
Articulos de INST.DE MEDICINA EXPERIMENTAL
Citación
Trucco, Lucas Daniel; Roselli, Emiliano; Araya, Paula; Nuñez, Nicolás Gonzalo; Mena, Hebe Agustina; et al.; Downregulation of adaptor protein MyD88 compromises the angiogenic potential of B16 murine melanoma; Public Library of Science; Plos One; 12; 6; 6-2017; 1-18; e0179897
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