Ron-receptor tyrosine kinase in tumorigenesis and metastasis.
Ron-receptor tyrosine kinase in tumorigenesis and metastasis.
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DOI：
10.2217/14796694.3.4.441
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发表时间：
2007-08-01
期刊：
影响因子：
--
通讯作者：
Waltz, Susan E
中科院分区：
文献类型：
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作者：
Leonis, Mike A;Thobe, Megan N;Waltz, Susan E
在过去的十年中，Ron受体酪氨酸激酶因其潜在的致癌作用而被越来越多的人认识。RON受体的激活导致共同受体酪氨酸激酶下游信号通路的激活，尤其是在肿瘤模型中，MAPK、PI3K和β-连环蛋白的激活。许多哺乳动物肿瘤发生的实验模型已经证明，RON受体活性的增加与多种上皮性器官的肿瘤发生有关。越来越多的证据表明RON是人类肿瘤生物学中的癌基因。在大量的人类肿瘤中，RON受体过度表达和过度激活，并且RON的过度表达与至少两种人类癌症状态的患者的临床预后相关，即乳腺癌和膀胱癌。几种实验方法已经被证明成功地阻断了RON的活性和功能，鉴于这些令人信服的数据，在靶向人类癌症中阻断RON受体活性的方法应该被证明在未来的临床研究试验中是卓有成效的。
The Ron-receptor tyrosine kinase has been increasingly recognized for its tumorigenic potential in the last decade. Ron-receptor activation leads to the activation of common receptor tyrosine kinase downstream-signaling pathways, and most prominently in tumor models, activation of MAPK, PI3K and beta-catenin. Numerous experimental models of mammalian tumorigenesis have demonstrated that increased Ron-receptor activity correlates with increased tumorigenesis in a variety of organs of epithelial origin. The evidence for Ron as an oncogene in human tumor biology is growing. The Ron receptor is overexpressed and over activated in a large number of human tumors, and overexpression of Ron correlates with a worse clinical outcome for patients in at least two human cancer states, namely breast and bladder cancer. Several experimental approaches have been demonstrated to successfully block Ron activity and function, and given these convincing data, approaches to block Ron-receptor activity in targeted human cancers should prove to be fruitful in the setting of future clinical research trials.