Coenzyme Q₀ Enhances Ultraviolet B–Induced Apoptosis in Human Estrogen Receptor–Positive Breast (MCF-7) Cancer Cells

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