Colorectal cancer is a major cause of morbidity and mortality that accounts for over 9% of all incidences of cancer. Additionally, colorectal cancer is widely recognized as an environmental disease related to ill-defined cultural, social and lifestyle factors including physical activity, obesity, cigarette smoking and heavy alcohol consumption. Accordingly, natural phytochemicals and extracts have attracted attention because of their beneficial biological effects. Coenzyme Q10 (CoQ10) is a common supplementary medicine applied to increase bioenergetic capacity in various diseases. Therefore, in this study, we investigated whether CoQ10 treatment has any inhibitory effects and its related cellular mechanisms in human colon cancer HCT116 cells. A MTT assay revealed that CoQ10 slightly decreased the proliferation of HCT116 cells; however, glutathione- and superoxide dismutase- activity were unchanged in response to CoQ10 treatment. A DCF-DA assay revealed that CoQ10 slightly increased ROS release of HCT116 cells. However, in a nitric oxide (NO) assay, CoQ10 significantly increased NO production in a dose-dependent manner. The results of western blot analysis revealed that the protein levels of Bax, p21 and p53 were increased, whereas the protein level of Bcl2 was decreased suggesting that the CoQ10-mediated inhibitory mechanism is associated with apoptotic signaling. Taken together, our findings indicate that CoQ10 has an inhibitory effect on the growth of colon cancer cells via NO production that is associated with regulation of factors involved in apoptotic signaling including Bax, Bcl2, p21 and p53.

Abstract
 INTRODUCTION
 MATERIALS AND METHODS
  Materials
  Cell culture and treatment
  MTT assay
  Glutathione (GSH) and Superoxide Dismutase (SOD)assay
  DCF-DA flow cytometric analysis
  Nitric oxide (NO) assay
  Western blot analysis
  Statistical analysis
 RESULTS
  Morphology and cell viability of HCT116 cells in thetreatment of CoQ10
  Cellular ROS and NO production of HCT116 cells inthe treatment of CoQ10
  CoQ10-induced cellular apoptosis in HCT116 cells
 DISCUSSION
 REFERENCES

• Se-Ran Yang(Department of Thoracic and Cardiovascular Surgery, School of Medicine, Kangwon National University) Corresponding Author
• Soojin Jang(Department of Thoracic and Cardiovascular Surgery, School of Medicine, Kangwon National University)
• Jooyeon Lee(Department of Thoracic and Cardiovascular Surgery, School of Medicine, Kangwon National University)
• Se Min Ryu(Department of Thoracic and Cardiovascular Surgery, School of Medicine, Kangwon National University)
• Hanbyeol Lee(Department of Thoracic and Cardiovascular Surgery, School of Medicine, Kangwon National University)
• Jeong-Ran Park(Department of Thoracic and Cardiovascular Surgery, School of Medicine, Kangwon National University)
• Aera Jang(Department of Animal Products and Food Science, Kangwon National University) Corresponding Author
• Dongwook Kim(Department of Animal Products and Food Science, Kangwon National University)
• Hyejin Kim(Department of Animal Products and Food Science, Kangwon National University)