ADAMTS1 Supports Endothelial Plasticity of Glioblastoma Cells with Relevance for Glioma Progression

被引:6
|
作者
Serrano-Garrido, Orlando [1 ,2 ]
Peris-Torres, Carlos [1 ]
Redondo-Garcia, Silvia [1 ]
Asenjo, Helena G. [1 ]
Plaza-Calonge, Maria del Carmen [1 ]
Fernandez-Luna, Jose Luis [3 ]
Rodriguez-Manzaneque, Juan Carlos [1 ]
机构
[1] Univ Granada, Ctr Genom & Oncol Res Pfizer, Junta Andalucia, GENYO, Ave Ilustrac,114, Granada 18016, Spain
[2] Univ Panama, Fac Med, Ciudad Univ, Panama City 3366, Panama
[3] Hosp Univ Marques Valdecilla, Mol Genet Unit, Ave Valdecilla,S-N, Santander 39008, Spain
关键词
ADAMTS proteases; endothelial-like phenotype; extracellular metalloprotease; glioblastoma; plasticity;
D O I
10.3390/biom11010044
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Gliomas in general and the more advanced glioblastomas (GBM) in particular are the most usual tumors of the central nervous system with poor prognosis. GBM patients develop resistance to distinct therapies, in part due to the existence of tumor cell subpopulations with stem-like properties that participate in trans-differentiation events. Within the complex tumor microenvironment, the involvement of extracellular proteases remains poorly understood. The extracellular protease ADAMTS1 has already been reported to contribute to the plasticity of cancer cells. Accordingly, this basic knowledge and the current availability of massive sequencing data from human gliomas, reinforced the development of this work. We first performed an in silico study of ADAMTS1 and endothelial markers in human gliomas, providing the basis to further assess these molecules in several primary glioblastoma-initiating cells and established GBM cells with the ability to acquire an endothelial-like phenotype. Using a co-culture approach of endothelial and GBM cells, we noticed a relevant function of ADAMTS1 in GBM cells leading the organization of endothelial-like networks and, even more significantly, we found a blockade of the formation of tumor-spheres and a deficient response to hypoxia in the absence of ADAMTS1. Our data support a chief role of this protease modulating the phenotypic plasticity of GBM.
引用
收藏
页码:1 / 17
页数:17
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