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

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.

Anti-EMT properties of CoQ0 attributed to PI3K/AKT/NFKB/MMP-9 signaling pathway through ROS-mediated apoptosis

“…It possesses strong antioxidant activity and prevents the mitochondrial permeability transition pore [18] from being opened calcium-dependently. CoQ 0 has demonstrated activity against the proliferation of numerous cancer cell lines (e.g., HepG2, A549, and SW480) [19, 20]. Although it exhibits cytotoxic anticancer activities, it was also demonstrated to stimulate insulin secretion in pancreatic islets [21].…”

Effect of antioxidants coenzyme Q10 and β‑carotene on the cytotoxicity of vemurafenib against human malignant melanoma

“…It is also known that 300 mg per day is a common dosage of commercial products of coenzyme Q10 ( 81 ). Published research used coenzyme Q10 at concentrations from 5–60 µM ( 64 , 82 , 83 ). The present study used CoQ10 at concentrations of 1, 5 and 10 µM that are achievable in the plasma of CoQ10 supplement-consuming individuals.…”

“…Since cancer cells perform high-level metabolic activity and suffer from more oxidative stress ( 63 ), antioxidants could potentially promote the growth and progression of cancers by mopping up free radicals from cancer cells. In fact, our previous research has demonstrated that antioxidant vitamin C exerted a stimulatory effect at physiological concentration on the growth and metastasis of human malignant melanoma ( 64 ).…”

“…In the present study, we hypothesized that the antioxidants CoQ-10 and β-carotene have an effect on the growth and invasiveness of human malignant melanoma cells. In addition, in a previous study our lab demonstrated that the BRAF kinase inhibitor vemurafenib, an FDA-approved antimelanoma drug, increased the oxidative stress in human malignant melanoma cells ( 64 ); thus antioxidants may interfere with the cytotoxic effect of vemurafenib on melanoma cells by scavenging free radicals. Hence, the present study aimed to determine the effect of CoQ-10 and β-carotene on the growth, migration and invasion and apoptosis induction of human malignant melanoma cell lines, and also on the cytotoxicity of emurafenib on human malignant melanoma cells.…”

Coenzyme Q0 From Antrodia cinnamomea Exhibits Drug-Resistant Bacteria Eradication and Keratinocyte Inflammation Mitigation to Ameliorate Infected Atopic Dermatitis in Mouse

“…It belongs to the family of coenzyme Q consisting of a benzoquinone structure conjugated to an isoprenoid chain from C0 to C10. CoQ 0 has the potential activity to suppress inflammation, cancer, and metabolic diseases (Wang et al, 2017). The inhibitory effect of CoQ 0 on S. aureus development has also been reported in previous studies (Fan et al, 2019).…”