Department of Biochemistry and Molecular Genetics, University of Illinois at Chicago, USA.
Department of Biochemistry and Molecular Genetics, University of Illinois at Chicago, USA; University of Illinois Cancer Center, University of Illinois at Chicago, USA.
Biochim Biophys Acta Rev Cancer. 2020 Dec;1874(2):188432. doi: 10.1016/j.bbcan.2020.188432. Epub 2020 Sep 18.
Protein tyrosine kinase 6 (PTK6) is the most well studied member of the PTK6 family of intracellular tyrosine kinases. While it is expressed at highest levels in differentiated cells in the regenerating epithelial linings of the gastrointestinal tract and skin, induction and activation of PTK6 is detected in several cancers, including breast and prostate cancer where high PTK6 expression correlates with worse outcome. PTK6 expression is regulated by hypoxia and cell stress, and its kinase activity is induced by several growth factor receptors implicated in cancer including members of the ERBB family, IGFR1 and MET. Activation of PTK6 at the plasma membrane has been associated with the epithelial mesenchymal transition and tumor metastasis. Several lines of evidence indicate that PTK6 has context dependent functions that depend on cell type, intracellular localization and kinase activation. Systemic disruption of PTK6 has been shown to reduce tumorigenesis in mouse models of breast and prostate cancer, and more recently small molecule inhibitors of PTK6 have exhibited efficacy in inhibiting tumor growth in animal models. Here we review data that suggest targeting PTK6 may have beneficial therapeutic outcomes in some cancers.
蛋白酪氨酸激酶 6(PTK6)是细胞内酪氨酸激酶家族中研究最为广泛的成员之一。虽然它在胃肠道和皮肤的再生上皮衬里中分化程度最高的细胞中表达水平最高,但在包括乳腺癌和前列腺癌在内的几种癌症中都检测到了 PTK6 的诱导和激活,在这些癌症中,高 PTK6 表达与预后较差相关。PTK6 的表达受缺氧和细胞应激调节,其激酶活性可被几种生长因子受体诱导,包括 ERBB 家族、IGFR1 和 MET 成员。PTK6 在质膜上的激活与上皮间质转化和肿瘤转移有关。有几条证据表明,PTK6 具有依赖于细胞类型、细胞内定位和激酶激活的上下文相关功能。在乳腺癌和前列腺癌的小鼠模型中,全身性破坏 PTK6 已被证明可减少肿瘤发生,最近,PTK6 的小分子抑制剂在动物模型中表现出抑制肿瘤生长的功效。在这里,我们回顾了一些数据,这些数据表明针对 PTK6 可能在某些癌症中具有有益的治疗效果。