Targeting catalase but not peroxiredoxins enhances arsenic trioxide-induced apoptosis in K562 cells.
Targeting catalase but not peroxiredoxins enhances arsenic trioxide-induced apoptosis in K562 cells.
复制标题
靶向过氧化氢酶而非过氧化还原蛋白可增强三氧化二砷诱导的 K562 细胞凋亡。
DOI：
10.1371/journal.pone.0104985
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Wu YL
中科院分区：
文献类型：
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作者：
Song LL;Tu YY;Xia L;Wang WW;Wei W;Ma CM;Wen DH;Lei H;Xu HZ;Wu YL
Despite considerable efficacy of arsenic trioxide (As2O3) in acute promyelocytic leukemia (APL) treatment, other non-APL leukemias, such as chronic myeloid leukemia (CML), are less sensitive to As2O3 treatment. However, the underlying mechanism is not well understood. Here we show that relative As2O3-resistant K562 cells have significantly lower ROS levels than As2O3-sensitive NB4 cells. We compared the expression of several antioxidant enzymes in these two cell lines and found that peroxiredoxin 1/2/6 and catalase are expressed at high levels in K562 cells. We further investigated the possible role of peroxirdoxin 1/2/6 and catalase in determining the cellular sensitivity to As2O3. Interestingly, knockdown of peroxiredoxin 1/2/6 did not increase the susceptibility of K562 cells to As2O3. On the contrary, knockdown of catalase markedly enhanced As2O3-induced apoptosis. In addition, we provide evidence that overexpression of BCR/ABL cannot increase the expression of PRDX 1/2/6 and catalase. The current study reveals that the functional role of antioxidant enzymes is cellular context and treatment agents dependent; targeting catalase may represent a novel strategy to improve the efficacy of As2O3 in CML treatment.
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影响因子：
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