Coenzyme Q0Enhances Ultraviolet B-Induced Apoptosis in Human Estrogen Receptor-Positive Breast (MCF-7) Cancer Cells.
Coenzyme Q0(CoQ0; 2,3-dimethoxy-5-methyl-1,4-benzoquinone), a major active constituent of Antrodia camphorata, has been shown to inhibit human triple-negative breast cancer (MDA-MB-231) cells through induction of apoptosis and cell-cycle arrest. Ecological studies have suggested a possible association between ultraviolet B (UVB) radiation and reduction in the risk of breast cancer. However, the underlying mechanism of the combination of CoQ0and UVB in human estrogen receptor-positive breast cancer (MCF-7) remains unclear. In this study, the possible effect of CoQ0on inducing apoptosis in MCF-7 cells under exposure to low-dose UVB (0.05 J/cm2) has been investigated. CoQ0treatment (0-35 µM, for 24-72 hours) inhibits moderately the growth of breast cancer MCF-7 cells, and the cell viability was significantly decreased when the cells were pretreated with UVB irradiation. It was noted that there was a remarkable accumulation of subploid cells, the so-called sub-G1 peak, in CoQ0-treated cells by using flow cytometric analysis, which suggests that the viability reduction observed after treatment may result from apoptosis induction in MCF-7 cells. CoQ0caused an elevation of reactive oxygen species, as indicated by dichlorofluorescein fluorescence, and UVB pretreatment significantly increased CoQ0-induced reactive oxygen species generation in MCF-7 cells. In addition, cells were exposed to CoQ0, and the induction of DNA damage was evaluated by single-cell gel electrophoresis (comet assay). CoQ0-induced DNA damage was remarkably enhanced by UVB pretreatment. Furthermore, CoQ0induced apoptosis in MCF-7 cells, which was associated with PARP degradation, Bcl-2/Bax dysregulation, and p53 expression as shown by western blot. Collectively, these findings suggest that CoQ0might be an important supplemental agent for treating patients with breast cancer.
1 National Chung Hsing University, Taichung, Taiwan.
Hui-Min
HM
Wang
2 China Medical University, Taichung, Taiwan.
Hsin-Ling
HL
Yang
2 China Medical University, Taichung, Taiwan.
Varadharajan
V
Thiyagarajan
2 China Medical University, Taichung, Taiwan.
Tzu-Hsiang
TH
Huang
3 Asia University, Taichung, Taiwan.
Pei-Jane
PJ
Huang
4 National Central University, Chung-Li, Taiwan.
Ssu-Ching
SC
Chen
2 China Medical University, Taichung, Taiwan.
Jer-Yuh
JY
Liu
5 Chung Shan Medical University, Taichung, Taiwan.
Li-Sung
LS
Hsu
1 National Chung Hsing University, Taichung, Taiwan.|6 Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Hsueh-Wei
HW
Chang
2 China Medical University, Taichung, Taiwan.|3 Asia University, Taichung, Taiwan.
You-Cheng
YC
Hseu
D017209:Apoptosis / Q000187:drug effects*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism; D059447:Cell Cycle Checkpoints / Q000187:drug effects; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D004249:DNA Damage / Q000187:drug effects; D005260:Female; D006801:Humans; D061986:MCF-7 Cells; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D011960:Receptors, Estrogen / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014451:Ubiquinone / Q000494:pharmacology*; D014466:Ultraviolet Rays / Q000009:adverse effects*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D011960:Receptors, Estrogen; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; D014451:Ubiquinone; D011065:Poly(ADP-ribose) Polymerases
CoQ0; ROS; apoptosis; breast cancer; chemotherapy; ultraviolet B