Cancer therapy: can the challenge be MET?

被引:202
作者
Corso, S [1 ]
Comoglio, PM [1 ]
Giordano, S [1 ]
机构
[1] Univ Turin, Sch Med, IRCC, Inst Canc Res & Treatment,Div Mol Oncol, I-10060 Turin, Italy
关键词
D O I
10.1016/j.molmed.2005.04.005
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
The deregulation of tyrosine kinase receptors (RTKs) is frequent in human tumors and is often associated with the acquisition of an aggressive phenotype. The Met oncogene, encoding the RTK for hepatocyte growth factor (HGF), controls genetic programs leading to cell growth, invasion and protection from apoptosis. The deregulated activation of Met is crucial not only for the acquisition of tumorigenic properties but also to achieve an invasive phenotype. The involvement of MET in human tumors has been definitively established and can be achieved through several mechanisms, including MET interaction with unrelated membrane receptors, such as integrins, plexins, CD44, FAS and other RTKs. Interfering with Met activation is thus a new and challenging approach to hamper tumorigenic and metastatic processes.
引用
收藏
页码:284 / 292
页数:9
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