Netrin-1 in glioblastoma neovascularization: the new partner in crime?
Author
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Vásquez Moya, Ximena del Pilar
Author
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Sánchez Gómez, Pilar
Author
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Palma Alvarado, Veronica Alejandra
Admission date
dc.date.accessioned
2021-11-24T20:11:42Z
Available date
dc.date.available
2021-11-24T20:11:42Z
Publication date
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2021
Cita de ítem
dc.identifier.citation
Int. J. Mol. Sci. 2021, 22(15)
es_ES
Identifier
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10.3390/ijms22158248
Identifier
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https://repositorio.uchile.cl/handle/2250/182875
Abstract
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Glioblastoma (GBM) is the most aggressive and common primary tumor of the central nervous system. It is characterized by having an infiltrating growth and by the presence of an excessive and aberrant vasculature. Some of the mechanisms that promote this neovascularization are angiogenesis and the transdifferentiation of tumor cells into endothelial cells or pericytes. In all these processes, the release of extracellular microvesicles by tumor cells plays an important role. Tumor cell-derived extracellular microvesicles contain pro-angiogenic molecules such as VEGF, which promote the formation of blood vessels and the recruitment of pericytes that reinforce these structures. The present study summarizes and discusses recent data from different investigations suggesting that Netrin-1, a highly versatile protein recently postulated as a non-canonical angiogenic ligand, could participate in the promotion of neovascularization processes in GBM. The relevance of determining the angiogenic signaling pathways associated with the interaction of Netrin-1 with its receptors is posed. Furthermore, we speculate that this molecule could form part of the microvesicles that favor abnormal tumor vasculature. Based on the studies presented, this review proposes Netrin-1 as a novel biomarker for GBM progression and vascularization.
es_ES
Patrocinador
dc.description.sponsorship
Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT)
CONICYT FONDECYT 1140697
Ministerio de Ciencia, Innovacion y Universidades and FEDER funds RTI2018-093596
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Lenguage
dc.language.iso
en
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Publisher
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MDPI
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Type of license
dc.rights
Attribution-NonCommercial-NoDerivs 3.0 United States