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

Hui Min Wang, Hsin Ling Yang, Varadharajan Thiyagarajan, Tzu Hsiang Huang, Pei Jane Huang, Ssu Ching Chen, Jer Yuh Liu, Li Sung Hsu, Hsueh Wei Chang, You Cheng Hseu

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

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.

Original languageEnglish
Pages (from-to)385-396
Number of pages12
JournalIntegrative Cancer Therapies
Volume16
Issue number3
DOIs
StatePublished - 1 Sep 2017

Keywords

  • CoQ
  • ROS
  • apoptosis
  • breast cancer
  • chemotherapy
  • ultraviolet B

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