PUMA overexpression induces reactive oxygen species generation and proteasome-mediated stathmin degradation in colorectal cancer cells

被引:110
|
作者
Liu, ZH
Lu, HM
Shi, HL
Du, YC
Yu, J
Gu, S
Chen, M
Liu, KJ
Hu, CAA
机构
[1] Univ New Mexico, Dept Biochem & Mol Biol, Sch Med, Albuquerque, NM 87131 USA
[2] Univ New Mexico, Ctr Hlth Sci, EPR Ctr, Albuquerque, NM 87131 USA
[3] Univ New Mexico, Ctr Hlth Sci, Toxicol Program, Albuquerque, NM 87131 USA
[4] Los Alamos Natl Lab, Div Biosci, Los Alamos, NM USA
[5] Univ Pittsburgh, Dept Pathol, Inst Canc, Pittsburgh, PA USA
关键词
D O I
10.1158/0008-5472.CAN-04-1754
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Increased amounts of reactive oxygen species (ROS) induce apoptosis in mammalian cells. PUMA (P53 up-regulated modulator of apoptosis), a mitochondrial proapoptotic BH3-only protein, induces rapid apoptosis through a Bax- and mitochondria-dependent pathway. However, the molecular basis of PUMA-induced apoptosis is largely not understood. Using a combination of biophysical and biochemical methods and PUMA-inducible colorectal cells, DLD-1.PUMA, we showed that (a) PUMA-induced apoptosis is dose and time dependent; (b) PUMA-induced apoptosis is directly associated with ROS generation; (c) diphenyleneiodonium, chloride, a ROS blocker, or BAX-inhibiting peptide, a suppressor of BAX translocation, decreased ROS generation and apoptosis in DLD-1.PUMA cells; (d) overexpression of PUMA induced up-regulation (>1.34-fold) of peroxiredoxin I and down-regulation (by 25%) of stathmin through proteasome-mediated degradation; and (e) hydrogen peroxide down-regulated stathmin and disrupted the cellular microtubule network Our findings indicate that PUMA induces apoptosis, in part, through the BAX-dependent generation of superoxide and hydrogen peroxide. ROS overproduction and oxidative stress induce proteome-wise alterations, such as stathmin degradation and disorganization of the cell microtubule network, in apoptotic cells.
引用
收藏
页码:1647 / 1654
页数:8
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