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Extracellular matrix components in breast cancer progression and metastasis
被引:213
|作者:
Oskarsson, Thordur
[1
,2
,3
]
机构:
[1] Heidelberg Inst Stem Cell Technol & Expt Med HI S, D-69120 Heidelberg, Germany
[2] German Canc Res Ctr, Div Stem Cells & Canc, D-69120 Heidelberg, Germany
[3] German Canc Consortium DKTK, Heidelberg, Germany
来源:
关键词:
Extracellular matrix;
Metastatic niche;
Mammary gland involution;
Tissue remodeling;
Metastatic breast cancer;
Therapy resistance;
INVOLUTING MAMMARY-GLAND;
CARCINOMA IN-SITU;
TENASCIN-C;
BONE METASTASES;
OSTEOPONTIN EXPRESSION;
PLASMINOGEN-ACTIVATOR;
PLASMA OSTEOPONTIN;
TUMOR PROGRESSION;
EPITHELIAL-CELLS;
LYSYL OXIDASE;
D O I:
10.1016/j.breast.2013.07.012
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
The extracellular matrix (ECM) is composed of highly variable and dynamic components that regulate cell behavior. The protein composition and physical properties of the ECM govern cell fate through biochemical and biomechanical mechanisms. This requires a carefully orchestrated and thorough regulation considering that a disturbed ECM can have serious consequences and lead to pathological conditions like cancer. In breast cancer, many ECM proteins are significantly deregulated and specific matrix components promote tumor progression and metastatic spread. Intriguingly, several ECM proteins that are associated with breast cancer development, overlap substantially with a group of ECM proteins induced during the state of tissue remodeling such as mammary gland involution. Fibrillar collagens, fibronectin, hyaluronan and matricellular proteins are matrix components that are common to both involution and cancer. Moreover, some of these proteins have in recent years been identified as important constituents of metastatic niches in breast cancer. In addition, specific ECM molecules, their receptors or enzymatic modifiers are significantly involved in resistance to therapeutic intervention. Further analysis of these ECM proteins and the downstream ECM mediated signaling pathways may provide a range of possibilities to identify druggable targets against advanced breast cancer. (C) 2013 Elsevier Ltd. All rights reserved.
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页码:S66 / S72
页数:7
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