期刊
CANCER LETTERS
卷 338, 期 2, 页码 185-192出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2013.04.004
关键词
ACK1; TNK2; AKT; Tyrosine kinase; Small molecule inhibitor; Drug resistance
类别
资金
- Department of Defense [W81XWH-12-1-0248, PC121661, PC121355]
- National Cancer Institute, NIH [1R01CA135328]
- Moffitt Lung Cancer Spore
ACK1 tyrosine kinase, located on chromosome 3q29, is aberrantly activated, amplified or mutated in a wide variety of human cancers. While the deregulated kinase is oncogenic and its activation correlates with progression to metastatic stage, its inhibition causes cell cycle arrest, sensitizes cells to ionizing radiation and induces apoptosis. Oncogenicity of ACK1 is not only due to its ability to promote activation of critical pro-survival kinases and harmone receptors by phosphorylating at distinct tyrosine residues, but also by employing a similar mechanism to eliminate a tumor suppressor from cancer cells. Despite the substantial data supporting the oncogenic role of ACK1, and the potential clinical benefit of blocking ACK1 in metastatic disease, to date ACK1-specific small molecule inhibitors have not been exploited for cancer therapy. This review highlights recent advances that elucidate how cancer cells employ ACK1 kinase to their advantage and discusses some of the novel ACK1 inhibitors that have shown promise in pre-clinical studies. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据