FAK in cancer: mechanistic findings and clinical applications.
FAK in cancer: mechanistic findings and clinical applications.
复制标题
DOI：
10.1038/nrc3792
复制
发表时间：
2014-09
期刊：
影响因子：
--
通讯作者：
中科院分区：
文献类型：
--
作者：
粘着斑激酶（FAK）是一种细胞质蛋白酪氨酸激酶，在几种晚期实体癌中过度表达和激活。FAK通过作用于癌细胞以及肿瘤微环境的基质细胞来促进肿瘤进展和转移。FAK的激酶依赖性和非依赖性功能控制细胞运动、侵袭、存活、基因表达和癌症干细胞自我更新。小分子FAK抑制剂在几种临床前模型中降低肿瘤生长和转移，并在不良事件有限的患者中具有初始临床活性。我们讨论了FAK信号对肿瘤和基质细胞生物学的影响，为未来的治疗机会提供了理论基础和支持。
Focal adhesion kinase (FAK) is a cytoplasmic protein tyrosine kinase that is over-expressed and activated in several advanced-stage solid cancers. FAK promotes tumor progression and metastasis through effects on cancer cells, as well as stromal cells of the tumor microenvironment. FAK’s kinase-dependent and –independent functions control cell movement, invasion, survival, gene expression, and cancer stem cell self-renewal. Small molecule FAK inhibitors decrease tumor growth and metastasis in several preclinical models and possess initial clinical activity in patients with limited adverse events. We discuss FAK signaling effects on both tumor and stromal cell biology that provide rationale and support for future therapeutic opportunities.