氧化应激在调节慢性髓性白血病细胞系未折叠蛋白反应活性中的作用
Role of Oxidative Stress in Modulating Unfolded Protein Response Activity in Chronic Myeloid Leukemia Cell Line.
作者信息
Bazi Ali, Keramati Mohammad Reza, Gholamin Mehran
机构信息
Cancer Molecular Pathology Research Center, Imam Reza Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Faculty of Allied Medical Sciences, Zabol University of Medical Sciences, Zabol, Iran.
出版信息
Iran Biomed J. 2016;20(1):63-7. doi: 10.7508/ibj.2016.01.009. Epub 2015 Oct 3.
UNLABELLED
Recently, it has been revealed that tyrosine kinase inhibitors (TKIs) act through inducing both oxidative and endoplasmic reticulum (ER) stress in chronic myeloid leukemia cells. However, ER stress signaling triggers both apoptotic and survival processes within cells. Nevertheless, mechanisms by which TKIs avoid the pro-survival effects are not clear. The aim of this study was to evaluate the potential role of oxidative stress in activity of unfolded protein response (UPR) survival pathway within K562 cell line.
METHODS
The expression of UPR survival target genes, Xbp1, and Grp94 (glucose requiring protein 94) was studied in single and combined exposure to oxidative and ER stress in K562 cell line by quantitative and qualitative PCR.
RESULTS
The expression of UPR-related survival gene Grp94 was hampered by exposing to oxidative stress in cell induced with ER stress.
CONCLUSION
Interaction of oxidative and ER stress may role as a mediator influencing UPR signaling activity.
未标记
最近发现，酪氨酸激酶抑制剂（TKIs）通过在慢性髓性白血病细胞中诱导氧化应激和内质网（ER）应激发挥作用。然而，内质网应激信号在细胞内触发凋亡和存活过程。尽管如此，酪氨酸激酶抑制剂避免促存活效应的机制尚不清楚。本研究的目的是评估氧化应激在K562细胞系中未折叠蛋白反应（UPR）存活途径活性中的潜在作用。
方法
通过定量和定性PCR研究K562细胞系在单独及联合暴露于氧化应激和内质网应激时，UPR存活靶基因Xbp1和Grp94（葡萄糖需求蛋白94）的表达。
结果
在内质网应激诱导的细胞中，暴露于氧化应激会阻碍UPR相关存活基因Grp94的表达。
结论
氧化应激和内质网应激的相互作用可能作为影响UPR信号活性的介质发挥作用。
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