Notch increases the shedding of HB-EGF by ADAM12 to potentiate invadopodia formation in hypoxia

被引:116
作者
Diaz, Begona [1 ]
Yuen, Angela [1 ]
Iizuka, Shinji [1 ]
Higashiyama, Shigeki [2 ]
Courtneidge, Sara A. [1 ]
机构
[1] Sanford Burnham Med Res Inst, Ctr Canc, Tumor Microenvironm Program, La Jolla, CA 92037 USA
[2] Ehime Univ, Dept Cell Growth & Tumor Regulat, Proteomed Res Ctr, Toon City, Ehime 7910295, Japan
基金
美国国家卫生研究院;
关键词
INDUCIBLE FACTOR-I; BREAST-CANCER METASTASIS; E-CADHERIN EXPRESSION; GROWTH-FACTOR; GENE-EXPRESSION; MESSENGER-RNA; TUMOR-GROWTH; LUNG CARCINOMAS; CELL-MIGRATION; BINDING;
D O I
10.1083/jcb.201209151
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Notch regulates cell-cell contact-dependent signaling and is activated by hypoxia, a micro-environmental condition that promotes cellular invasion during both normal physiology and disease. The mechanisms by which hypoxia and Notch regulate cellular invasion are not fully elucidated. In this paper, we show that, in cancer cells, hypoxia increased the levels and activity of the ADAM12 metalloprotease in a Notch signaling-dependent manner, leading to increased ectodomain shedding of the epidermal growth factor (EGF) receptor (EGFR) ligand heparin-binding EGF-like growth factor. Released HB-EGF induced the formation of invadopodia, cellular structures that aid cancer cell invasion. Thus, we describe a signaling pathway that couples cell contact-dependent signaling with the paracrine activation of the EGFR, indicating cross talk between the Notch and EGFR pathways in promoting cancer cell invasion. This signaling pathway might regulate the coordinated acquisition of invasiveness by neighboring cells and mediate the communication between normoxic and hypoxic areas of tumors to facilitate cancer cell invasion.
引用
收藏
页码:279 / 292
页数:14
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