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首页> 外文期刊>Biochimica et biophysica acta. Reviews on cancer >Targeting protein tyrosine kinase 6 in cancer
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Targeting protein tyrosine kinase 6 in cancer

机译：靶向蛋白酪氨酸激酶6在癌症中

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摘要

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.
机译：蛋白质酪氨酸激酶6（PTK6）是PTK6细胞内酪氨酸激酶的最良好研究的成员。虽然它在胃肠道和皮肤的再生上皮衬里中的分化细胞中表达的最高水平，但在几种癌症中检测到PTK6的诱导和激活，包括乳腺癌和前列腺癌，其中高PTK6表达与更差的结果相关。 PTK6表达受缺氧和细胞应激调节，其激酶活性由涉及癌症的几种生长因子受体诱导，包括erbB家族，IGFR1和满足的成员。在血浆膜上活化PTK6已经与上皮间充质转变和肿瘤转移有关。几种证据表明PTK6具有依赖于细胞类型，细胞内定位和激酶激活的上下文依赖功能。 PTK6的全身破坏已被证明可以减少乳腺癌和前列腺癌的小鼠模型中的肿瘤发生，并且最近的PTK6的小分子抑制剂在抑制动物模型中抑制肿瘤生长的功效表现出疗效。在这里，我们审查表明靶向PTK6的数据可能在某些癌症中具有有益的治疗结果。

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