Original article


, 6:3

First online:

Open Access This content is freely available online to anyone, anywhere at any time.

PPARα modulates gene expression profiles of mitochondrial energy metabolism in oral tumorigenesis

  • Yi-Ping HuangAffiliated withDepartment of Physiology, College of Medicine, China Medical University
  • , Nai Wen ChangAffiliated withDepartment of Biochemistry, College of Medicine,, China Medical University Email author 


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.


Fenofibrate Oral cancer PPARα RT2 profiler PCR array