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Coenzyme Q0 Enhances Ultraviolet B–Induced Apoptosis in Human Estrogen Receptor–Positive Breast (MCF-7) Cancer Cells
| Content Provider | SAGE Publishing |
|---|---|
| Author | Wang, Hui-Min Yang, Hsin-Ling Thiyagarajan, Varadharajan Huang, Tzu-Hsiang Huang, Pei-Jane Chen, Ssu-Ching Liu, Jer-Yuh Hsu, Li-Sung Chang, Hsueh-Wei Hseu, You-Cheng |
| Copyright Year | 2016 |
| Abstract | 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 CoQ0 and UVB in human estrogen receptor–positive breast cancer (MCF-7) remains unclear. In this study, the possible effect of CoQ0 on inducing apoptosis in MCF-7 cells under exposure to low-dose UVB (0.05 J/cm2) has been investigated. CoQ0 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 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. CoQ0 caused 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, CoQ0 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 CoQ0 might be an important supplemental agent for treating patients with breast cancer. |
| Related Links | https://journals.sagepub.com/doi/pdf/10.1177/1534735416673907?download=true |
| Starting Page | 385 |
| Ending Page | 396 |
| Page Count | 12 |
| ISSN | 15347354 |
| Issue Number | 3 |
| Volume Number | 16 |
| Journal | Integrative Cancer Therapies (ICT) |
| e-ISSN | 1552695X |
| DOI | 10.1177/1534735416673907 |
| Language | English |
| Publisher | Sage Publications CA |
| Publisher Date | 2016-11-07 |
| Publisher Place | Los Angeles |
| Access Restriction | Open |
| Rights Holder | © The Author(s) 2016 |
| Subject Keyword | breast cancer ultraviolet B ROS CoQ0 apoptosis chemotherapy |
| Content Type | Text |
| Resource Type | Article |
| Subject | Complementary and Alternative Medicine Oncology |
