由KRAS驱动的活性氧簇促进恶性转化。
KRAS-driven ROS promote malignant transformation.
作者信息
Suh Yongjoon, Lee Su-Jae
机构信息
Department of Life Science; Research Institute for Natural Sciences; Hanyang University ; Seoul, Korea.
出版信息
Mol Cell Oncol. 2015 Jan 22;2(1):e968059. doi: 10.4161/23723548.2014.968059. eCollection 2015 Jan-Mar.
The mechanism underlying KRAS (Kirsten rat sarcoma viral oncogene homolog)-driven cellular transformation remains unclear because of the complexity of its downstream effectors. Park et al. recently reported that levels of reactive oxygen species (ROS) are increased by KRAS and are responsible for KRAS-driven malignant transformation, and further identified the signaling cascade involved as KRAS/p38/PDPK1/PKCδ/p47(phox)/NOX1. These findings provide new insight into the molecular mechanisms governing KRAS-driven malignant transformation.
由于KRAS（ Kirsten大鼠肉瘤病毒癌基因同源物）下游效应器的复杂性，其驱动细胞转化的机制仍不清楚。Park等人最近报道，活性氧（ROS）水平因KRAS升高，且这是KRAS驱动恶性转化的原因，并进一步确定了相关信号级联为KRAS/p38/PDPK1/PKCδ/p47（phox）/NOX1。这些发现为调控KRAS驱动恶性转化的分子机制提供了新见解。
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