Stellrecht Christine M, Gandhi Varsha
Department of Experimental Therapeutics, Unit 71, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA.
Cancer Lett. 2009 Jul 18;280(1):1-14. doi: 10.1016/j.canlet.2008.10.045. Epub 2008 Dec 18.
Tyrosine kinases are frequently deregulated in cancer either by constitutive activation, mutation, or over-expression. Though they are often associated with an aggressive phenotype they are also proving to be a druggable target. Activation of the MET receptor tyrosine kinase promotes cell proliferation, scattering, invasion, survival, and angiogenesis. Deregulation of MET promotes tumor formation, growth, progression, metastasis, and therapeutic resistance. Because MET is a player in so many aspects of cancer development and progression, it is a strong candidate for targeted therapy. Numerous agents have been developed that are able to target MET expression and/or function and are the focus of this review.
酪氨酸激酶在癌症中常常通过组成性激活、突变或过表达而失调。尽管它们通常与侵袭性表型相关，但它们也被证明是一个可成药的靶点。MET受体酪氨酸激酶的激活促进细胞增殖、分散、侵袭、存活和血管生成。MET的失调促进肿瘤形成、生长、进展、转移和治疗抗性。由于MET在癌症发展和进展的许多方面都发挥作用，它是靶向治疗的有力候选者。已经开发出许多能够靶向MET表达和/或功能的药物，这些药物是本综述的重点。
