氧化应激对食道鳞癌细胞能量代谢的影响
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Oxidative stress regulates cellular bioenergetics in
esophageal squamous cell carcinoma cell
背景与目的
本研究目的为观察CoCl2和H2O2诱导的氧化应激对食道鳞癌细胞株TE-1能量代谢调控的影响，并探讨其作用机制。
方 法
Western blot结果表明：经CoCl2和H2O2的处理，TE-1细胞线粒体呼吸链复合物亚基的表达显著减少，且细胞内活性氧（ROS）生成增加。
结 果
我们进一步用CoCl2（一种缺氧模拟试剂）处理TE-1细胞，发现处理后的TE-1细胞氧消耗率（OCR）明显下降且细胞外酸化率（ECAR）增加。但是，H2O2处理显著降低了线粒体呼吸和有氧糖酵解水平。此外，我们发现H2O2通过激活PARP、Caspase 3和Caspase 9，从而诱导TE-1细胞凋亡。
结 论
研究结果表明CoCl2和H2O2可通过上调ROS以及调控细胞能量代谢导致线粒体代谢功能障碍，从而影响肿瘤细胞的存活。
原始文献摘要
Zhang X, Lan L, Niu L, et al. Oxidative stress regulates cellular bioenergetics in esophageal squamous cell carcinoma cell:[J]. Biosci Rep, 2017, 37(6):BSR20171006.
The aim of the present study was to explore the effects of oxidative stress induced by CoCl2 and H2O2 on the regulation of bioenergetics of esophageal squamous cell carcinoma (ESCC) cell line TE-1 and analyze its underlying mechanism. Western blot results showed that CoCl2 and H2O2 treatment of TE-1 cells led to significant reduction in mitochondrial respiratory chain complex subunits expression and increasing intracellular reactive oxygen species (ROS) production.We further found that TE-1 cells treated with CoCl2, a hypoxia-mimicking reagent, dramatically reduced the oxygen consumption rate (OCR) and increased the extracellular acidification rate (ECAR). However, H2O2 treatment decreased both the mitochondrial respiration and aerobic glycolysis significantly. Moreover, we found that H2O2 induces apoptosis in TE-1 cells through the activation of PARP, Caspase 3, and Caspase 9. Therefore, our findings indicate that CoCl2 and H2O2 could cause mitochondrial dysfunction by up-regulation of ROS and regulating the cellular bioenergy metabolism, thus affecting the survival of tumor cells.
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