Abstract
Coenzyme Q(0) (CoQ(0); 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 CoQ(0) and UVB in human estrogen receptor-positive breast cancer (MCF-7) remains unclear. In this study, the possible effect of CoQ(0) on inducing apoptosis in MCF-7 cells under exposure to low-dose UVB (0.05 J/cm(2)) has been investigated. CoQ(0) treatment (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 CoQ(0)-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. CoQ(0) caused an elevation of reactive oxygen species, as indicated by dichlorofluorescein fluorescence, and UVB pretreatment significantly increased CoQ(0)-induced reactive oxygen species generation in MCF-7 cells. In addition, cells were exposed to CoQ(0), and the induction of DNA damage was evaluated by single-cell gel electrophoresis (comet assay). CoQ(0)-induced DNA damage was remarkably enhanced by UVB pretreatment. Furthermore, CoQ(0) induced 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 CoQ(0) might be an important supplemental agent for treating patients with breast cancer.