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논문 기본 정보

자료유형
학술저널
저자정보
장수진 (강원대학교) 이주연 (강원대학교) 류세민 (강원대학교) 이한별 (강원대학교) 박정란 (강원대학교 의학전문대학원 흉부외과) 김혜진 (강원대학교) 김동욱 (강원대학교) 장애라 (강원대학교) 양세란 (강원대학교)
저널정보
한국예방수의학회 예방수의학회지 예방수의학회지 제41권 제2호
발행연도
2017.6
수록면
59 - 65 (7page)
DOI
https://doi.org/10.13041/jpvm.2017.41.2.59

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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.

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