Downregulation of Protein Kinase Cα Was Involved in Selenite-Induced Apoptosis of NB4 Cells
Downregulation of Protein Kinase Cα Was Involved in Selenite-Induced Apoptosis of NB4 Cells
复制标题
DOI：
10.3727/096504010x12864748215089
复制
发表时间：
2010-01-01
影响因子：
3.1
通讯作者：
Xu, Cai-min
中科院分区：
文献类型：
--
作者：
Li, Zhu-shi;Shi, Ke-jian;Xu, Cai-min
我们在前期研究中发现，亚硒酸钠诱导人白血病NB 4细胞发生明显的凋亡，其中活性氧（ROS）、线粒体凋亡途径和内质网应激（ER stress）均参与其中。在本研究中，我们发现蛋白激酶C α（PKC α）显着下调亚硒酸盐诱导的细胞凋亡，这是由ROS介导的。此外，我们证实PKC α通过影响ERK 1/2和Akt发挥抗凋亡作用，而其下调则是在ROS的调节下通过caspase-3和PP 2Ac实现的。综上所述，我们推测在亚硒酸盐诱导的NB 4细胞凋亡中，PKC α起着对抗凋亡的作用，其下调可能是加重凋亡的机制之一。
We revealed in our previous research that sodium selenite induced obvious apoptosis of human leukemia NB4 cells, with reactive oxygen species (ROS), mitochondrial apoptosis pathway, and endoplasmic reticulum stress (ER stress) involved. In the present study, we revealed protein kinase C alpha (PKC alpha) was dramatically downregulated in selenite-induced apoptosis, which was mediated by ROS. Besides, we confirmed PKC alpha played an antiapoptotic role through its effects on ERK 1/2 and Akt, while its downregulation was attributed to caspase-3 and PP2Ac under the regulation of ROS. In summary, we speculated that in apoptosis of NB4 cells induced by selenite, PKC alpha functioned to counteract apoptosis, thus its downregulation seemed a mechanism aggravating apoptosis.