Autophagy inhibition through PI3K/Akt increases apoptosis by sodium selenite in NB4 cells
Autophagy inhibition through PI3K/Akt increases apoptosis by sodium selenite in NB4 cells
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DOI：
10.5483/bmbrep.2009.42.9.599
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发表时间：
2009-09-30
期刊：
影响因子：
3.8
通讯作者：
Xu, Caimin
中科院分区：
文献类型：
--
作者：
Ren, Yun;Huang, Fang;Xu, Caimin
硒具有诱导癌细胞凋亡的化疗特性，对正常细胞的副作用很小。然而，其机制尚不清楚。越来越多的证据表明，自噬和细胞凋亡之间存在重叠。在这项研究中，我们研究了自噬在硒诱导的NB4细胞凋亡中的作用。电镜、吖啶橙染色、western blot检测发现亚硒酸钠对NB4细胞的自噬有抑制作用，亚硒酸钠联合自噬抑制剂可上调细胞凋亡，下调PI3K/Akt信号通路。同样，当使用PI3K抑制剂时，自噬水平显著降低。综上所述，亚硒酸钠通过PI3K/Akt抑制自噬促进NB4细胞凋亡，抑制自噬有助于细胞凋亡的上调。[BMB报道2009年；42 (9): 599 - 604)
Selenium possesses the chemotherapeutic feature by inducing apoptosis in cancer cell with trivial side effects on normal cells. However, the mechanism in which is not clearly understood. Emerging evidence indicates the overlaps between the autophagy and the apoptosis. In this study, we have investigated the role of autophagy in selenium-induced apoptosis in NB4 cells. We find that autophagy is suppressed in NB4 cells treated by sodium selenite, as measured by electron microscope, acridine orange staining and western blot Moreover, selenite combined with autophagy inhibitor contributes to the up-regulation of apoptosis, while the PI3K/Akt signaling pathway is down- regulated. Consistently, when the inhibitor of PI3K was applied, the autophagic level significantly decreased. In summary, sodium selenite increases NB4 cell apoptosis by autophagy inhibition through PI3K/Akt and the inhibition of autophagy contributes to the up-regulation of apoptosis. [BMB reports 2009; 42(9): 599-604]