ROS-major mediators of extracellular matrix remodeling during tumor progression

被引:65
作者
Nikitovic, Dragana [1 ]
Corsini, Emanuela [2 ]
Kouretas, Dimitrios [3 ]
Tsatsakis, Aristidis [4 ]
Tzanakakis, George [1 ]
机构
[1] Univ Crete, Sch Med, Dept Histol Embryol, Iraklion 71003, Greece
[2] Univ Milan, Toxicol Lab, DiSFeB, I-20122 Milan, Italy
[3] Univ Thessaly, Dept Biochem & Biotechnol, Larisa, Greece
[4] Univ Crete, Dept Forens Sci & Toxicol, Iraklion 71003, Greece
关键词
Tumor; Metastasis; Extracellular matrix; ROS; Glycosaminoglycans; Matrix metalloproteinases; EPITHELIAL-MESENCHYMAL TRANSITION; ACTIVATOR RECEPTOR EXPRESSION; BREAST-CANCER CELLS; GROWTH-FACTOR-BETA; REACTIVE OXYGEN; OXIDATIVE STRESS; NITRIC-OXIDE; PLASMINOGEN-ACTIVATOR; FREE-RADICALS; NADPH OXIDASE;
D O I
10.1016/j.fct.2013.06.013
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Extracellular matrices (ECMs) represent a complex network of proteins, proteoglycans and glycosaminoglycans (GAGs), composed of independent structural domains, ultimately constituting the cell microenvironment. As a highly organized, insoluble suprastructure, the ECM can, in a spatially patterned and regulated manner, integrate and deliver multiple complex signals to cells that affect their behavior. During the progression of carcinogenesis, tumor cells, through a continually changing interface, remodel and simultaneously interact with the components of ECM, as well as with surrounding stromal cells. Within this complex network of ECM components affecting tumor progression, reactive oxygen species/reactive nitrogen species (ROS/RNS) play a wide emerging role. In this minireview we will focus on the ROS-dependent modulations of tumor ECM and how this in turn affects the insidious pathways of tumor progression and dissemination. (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码:178 / 186
页数:9
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