过氧化物酶体增殖物激活受体α（PPARα）在口腔肿瘤发生过程中调节线粒体能量代谢的基因表达谱。
PPARα modulates gene expression profiles of mitochondrial energy metabolism in oral tumorigenesis.
作者信息
Huang Yi-Ping, Chang Nai Wen
机构信息
Department of Physiology, College of Medicine, China Medical University, 404, Taichung, Taiwan.
Department of Biochemistry, College of Medicine,, China Medical University, 404, No. 91, Hsueh-Shih Road, Taichung, Taiwan.
出版信息
Biomedicine (Taipei). 2016 Mar;6(1):3. doi: 10.7603/s40681-016-0003-7. Epub 2016 Feb 10.
Metabolic reprogramming plays a crucial role in the development of cancer. The aim of this study was to explore the effect of fenofibrate, an agonist of peroxisome proliferator-activated receptor alpha (PPARα), on gene expression profiles of mitochondrial energy metabolism. Our results showed that PPARα expression was negatively correlated with tumor progression in an oral cancer mouse model. Activation of PPARα through fenofibrate suppressed migration of oral cancer cells. Differential protein profiling demonstrated that expressions of genes related to mitochondrial energy metabolism were either up-regulated (Atp5g3, Cyc1, Ndufa5, Ndufa10, and Sdhd) or down-regulated (Cox5b, Ndufa1, Ndufb7, and Uqcrh) through PPARα activation and response. Our results indicate that PPARα exhibits a great potential for anti-oral cancer therapies by modulating cancer cell mitochondrial energy metabolism.
代谢重编程在癌症发展中起着关键作用。本研究的目的是探讨过氧化物酶体增殖物激活受体α（PPARα）激动剂非诺贝特对线粒体能量代谢基因表达谱的影响。我们的结果表明，在口腔癌小鼠模型中，PPARα表达与肿瘤进展呈负相关。通过非诺贝特激活PPARα可抑制口腔癌细胞的迁移。差异蛋白质谱分析表明，通过PPARα激活和反应，与线粒体能量代谢相关的基因表达要么上调（Atp5g3、Cyc1、Ndufa5、Ndufa10和Sdhd），要么下调（Cox5b、Ndufa1、Ndufb7和Uqcrh）。我们的结果表明，PPARα通过调节癌细胞线粒体能量代谢在抗口腔癌治疗中具有巨大潜力。
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