Mitochondrial and Oxidative Stress-Mediated Activation of Protein Kinase D1 and Its Importance in Pancreatic Cancer.
Mitochondrial and Oxidative Stress-Mediated Activation of Protein Kinase D1 and Its Importance in Pancreatic Cancer.
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DOI：
10.3389/fonc.2017.00041
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发表时间：
2017
影响因子：
4.7
通讯作者：
Storz P
中科院分区：
文献类型：
--
作者：
Döppler H;Storz P
由于其代谢活性的改变和线粒体效率的降低，癌细胞经常表现出活性氧物种(ROS)的增加，但同时，为了避免细胞毒性信号和促进肿瘤发生信号，有适当的机制来控制ROS。这需要传递氧化应激增加的信号分子向细胞核发出信号，上调抗氧化基因。蛋白激酶D_1(PKD_1)，丝氨酸/苏氨酸激酶，就是这些ROS感受器之一。在这篇简短的综述中，我们重点介绍了PKD1如何被激活以响应氧化应激的机制，迄今已知的下游效应因子，以及PKD1启动的信号在胰腺癌发生发展中的重要性。
Due to alterations in their metabolic activity and decreased mitochondrial efficiency, cancer cells often show increased generation of reactive oxygen species (ROS), but at the same time, to avoid cytotoxic signaling and to facilitate tumorigenic signaling, have mechanism in place that keep ROS in check. This requires signaling molecules that convey increases in oxidative stress to signal to the nucleus to upregulate antioxidant genes. Protein kinase D1 (PKD1), the serine/threonine kinase, is one of these ROS sensors. In this mini-review, we highlight the mechanisms of how PKD1 is activated in response to oxidative stress, so far known downstream effectors, as well as the importance of PKD1-initiated signaling for development and progression of pancreatic cancer.