Signaling by Extracellular Vesicles Advances Cancer Hallmarks

被引:85
|
作者
Kanada, Masamitsu [1 ]
Bachmann, Michael H. [1 ]
Contag, Christopher H. [1 ,2 ,3 ]
机构
[1] Stanford Univ, Sch Med, Dept Pediat, Stanford, CA 94305 USA
[2] Stanford Univ, Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA
[3] Stanford Univ, Sch Med, Dept Radiol, Stanford, CA 94305 USA
来源
TRENDS IN CANCER | 2016年 / 2卷 / 02期
关键词
TUMOR-DERIVED MICROVESICLES; HYPOXIA-INDUCIBLE FACTORS; COMPETITIVE INTERACTIONS; INTERCELLULAR TRANSFER; TRANSFERRIN RECEPTOR; EMERGING ROLE; IN-VITRO; EXOSOMES; CELLS; PROMOTE;
D O I
10.1016/j.trecan.2015.12.005
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Mammalian cells secrete various extracellular vesicles (EVs; exosomes, microvesicles, and apoptotic bodies) that differ in biogenesis, composition, and function. Each vesicle type can originate from normal or cancerous cells, transfer molecular cargo to both neighboring and distant cells, and modulate cellular behaviors involved in eubiology and pathology, such as tumor development. Here, we review evidence for the role of EVs in the establishment and maintenance of cancer hallmarks, including sustaining proliferative signaling, evading growth suppression, resisting cell death, reprogramming energy metabolism, acquiring genomic instability, and remodeling the tumor microenvironment. We also discuss how EVs are implicated in the induction of angiogenesis, control of cellular invasion, initiation of premetastatic niches, maintenance of inflammation, and evasion of immune surveillance. The deeper understanding of the biology of EVs and their contribution to the development and progression of tumors is leading to new opportunities in the diagnosis and treatment of cancer.
引用
收藏
页码:84 / 94
页数:11
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