Coenzyme Q0 from Antrodia cinnamomea in Submerged Cultures Induces Reactive Oxygen Species‐Mediated Apoptosis in A549 Human Lung Cancer Cells

Chung, Ching‐Hu; Yeh, Szu-Chien; Chen, Chun‐Jen; Lee, Kung-Ta

doi:10.1155/2014/246748

Cited by 22 publications

(23 citation statements)

References 36 publications

(46 reference statements)

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“…Owing to its potent anticancer/cytotoxic properties against human breast cancer 25 , and lung cancer cells 40 , we assume that CoQ 0 could be a potential candidate to treat human ovarian carcinoma cells. For the first time, we have demonstrated that CoQ 0 , isolated from Antrodia camphorata , potently killed the ovarian SKOV-3 cancer cells and induced cell-cycle arrest via decreased cell-cycle regulatory proteins.…”

Section: Discussionmentioning

confidence: 99%

“…The cytotoxicity of CoQ 0 was associated with increased proportion of cells undergoing apoptosis, and this phenomenon was addressed by the induction of G 0 /G 1 cell-cycle arrest in MDA-MB-231 cells and S-phase arrest in SKBr3 cells 25 . CoQ 0 isolated from Antrodia cinnamomea submerged cultures has also reported to possess anticancer property by the decreased viability of A549, HepG2 and SW480 cancer cells, and increased ROS-mediated apoptosis 40 .…”

Section: Discussionmentioning

confidence: 99%

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Antitumor properties of Coenzyme Q0 against human ovarian carcinoma cells via induction of ROS-mediated apoptosis and cytoprotective autophagy

Hseu

Tsai

Korivi

et al. 2017

Sci Rep

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Coenzyme Q0 (CoQ0, 2,3-dimethoxy-5-methyl-1,4-benzoquinone) has been reported to exert anticancer properties against human breast/lung cancer cells. This study investigated the in vitro and in vivo anticancer properties of CoQ0 on human ovarian carcinoma (SKOV-3) cells and xenografted nude mice, and revealed the underlying molecular mechanism. CoQ0 induced G2/M arrest through downregulation of cyclin B1/A and CDK1/K2 expressions. CoQ0-induced autophagy as a survival mechanism was evidenced by increased accumulation of LC3-II, GFP-LC3 puncta, AVOs formation and Beclin-1/Bcl-2 dysregulation. Increased TUNEL-positive cells and Annexin-V/PI stained cells indicated CoQ0-induced late apoptosis. Both mitochondrial (caspase-3, PARP and Bax/Bcl-2 dysregulation) and ER stress (caspase-12 and Hsp70) signals are involved in execution of apoptosis. Interestingly, CoQ0-induced apoptosis/autophagy is associated with suppression of HER-2/neu and PI3K/AKT signalling cascades. CoQ0 triggered intracellular ROS production, whereas antioxidant N-acetylcysteine prevented CoQ0-induced apoptosis, but not autophagy. Inhibition of apoptosis by Z-VAD-FMK suppressed CoQ0-induced autophagy (diminished LC3-II/AVOs), indicates CoQ0-induced apoptosis led to evoke autophagy. Contrary, inhibition of autophagy by 3-MA/CQ potentiated CoQ0-induced apoptosis (increased DNA fragmentation/PARP cleavage). Furthermore, CoQ0 treatment to SKOV-3 xenografted nude mice reduced tumor incidence and burden. Histopathological analyses confirmed that CoQ0 modulated xenografted tumor progression by apoptosis induction. Our findings emphasize that CoQ0 triggered ROS-mediated apoptosis and cytoprotective autophagy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Antitumor properties of Coenzyme Q0 against human ovarian carcinoma cells via induction of ROS-mediated apoptosis and cytoprotective autophagy

Hseu

Tsai

Korivi

et al. 2017

Sci Rep

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“…With the global increase in antibiotic resistance and safety concerns surrounding the use of chlorine-based disinfectants, the antibacterial properties of plant-derived compounds are increasingly being investigated [40,41]. CoQ 0 , derived from A. cinnamomea, has attracted attention for its potential as a natural food preservative and as a therapeutic antibiotic [28]. Based on growth curve analysis, we identi ed appropriate SICs of CoQ 0 that had no effect on growth for use in subsequent assays.…”

Section: Discussionmentioning

confidence: 99%

“…Over the past decade, the use of plant-derived compounds as alternative antimicrobials has gained signi cant attention as a result of increasing concerns over the safety of synthetic antimicrobial agents and the emergence of antibiotic-resistant bacteria [27]. Coenzyme Q 0 (CoQ 0 ; 2,3-dimethoxy-5-methyl-1,4benzoquinone; C 9 H 10 O 4 ) is a benzoquinone compound extracted from the fungus Antrodia camphorata [28]. It has demonstrated anti-tumor, anti-in ammatory, and anti-angiogenic properties [29], as well as antibacterial activity against Staphylococcus aureus and Listeria monocytogenes [30,31].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Cronobacter Sakazakii Biofilm Formation and Expression of Virulence Factors by Coenzyme Q0

Guan¹,

Shi²,

Tong³

et al. 2020

Preprint

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Objectives：Here, we investigated the inhibitory effects of coenzyme Q0 (CoQ0) on biofilm formation and the expression of virulence genes by Cronobacter sakazakii. Results：We found that the minimum inhibitory concentration of CoQ0 against C. sakazakii strains ATCC29544 and ATCC29004 was 100 μg/mL, while growth curve assays showed that sub-inhibitory concentrations (SICs) of CoQ0 for both strains were 6.4, 3.2, 1.6 and 0.8 μg/mL. Assays exploring the inhibition of specific biofilm formation showed that SICs of CoQ0 inhibited biofilm formation by C. sakazakii in a dose-dependent manner, which was confirmed by scanning electron microscopy and confocal laser scanning microscopy analyses. CoQ0 inhibited the swimming and swarming motility of C. sakazakii and reduced its ability to adhere to and invade HT-29 cells. In addition, CoQ0 impeded the ability of C. sakazakii to survive and replicate within RAW 264.7 cells. Finally, real time polymerase chain reaction analysis confirmed that nine C. sakazakii genes associated with biofilm formation and virulence were down-regulated in response to CoQ0 treatment. Conclusion：Overall, our findings suggest that CoQ0 is a promising antibiofilm agent and provide new insights for the prevention and control of infections caused by C. sakazakii.

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“…Previous studies have reported that treatment with anti-tumor agents from different categories induce free radicals in non-tumor cells in both in vitro and in vivo (Weijl et al, 1997). Extracts of A. cinnamomea or its derived compounds induce apoptosis in cancer cells through reactive oxygen species (ROS) gen- eration following DNA damage (Chung et al, 2014;Yang et al, 2013). Thus, prior to the in vitro assay, the cytotoxic effect of LACC on CHO-K1 cells was examined by MTT assay.…”

Section: Mammalian Chromosome Aberration Testmentioning

confidence: 99%

In vitro and in vivo toxicological assessments of Antrodia cinnamomea health food product (Leader Antrodia cinnamomea Capsule)

Lin

Kumar

Vani

et al. 2016

Fundam. Toxicol. Sci.

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A unique medicinal mushroom Antrodia cinnamomea has been used for centuries to treat various human diseases. Recent studies revealed its potent pharmacological effects including anticancer, anti-inflammation, anti-oxidant, anti-diabetic, neuroprotection and hepatoprotection. The present study was aimed to investigate the toxicological effects of A. cinnamomea health food product "Leader Antrodia cinnamomea Capsule (LACC)" by measuring its genotoxic, oral toxic and teratotoxic effects in vitro and in vivo. Result of Ames test with 5 strains of Salmonella typhimurium shows no sign of increase in the numbers of revertant colonies upon exposure to LACC. Treatment of Chinese Hamster Ovary cells (CHO-K1) with LACC did not affect increase in the frequency of chromosomal aberration in vitro. In addition, treatment with LACC did not affect the proportions of immature to total erythrocytes and the number of micronuclei in the immature erythrocytes of ICR mice. Moreover, acute oral toxicity (14-days single-dose) or prolonged oral toxicity (28-and 90-days repeated oral dose) tests with rats showed that there were no observable adverse effects were found. Furthermore, teratological studies with LACC (500-2500 mg/kg/day) for 20 days, shows no observable segment II reproductive and developmental toxic evidences in pregnant SD rats and their fetus. These toxicological assessments strongly support the safety efficacy of LACC for human consumption.

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Coenzyme Q0 from Antrodia cinnamomea in Submerged Cultures Induces Reactive Oxygen Species‐Mediated Apoptosis in A549 Human Lung Cancer Cells

Cited by 22 publications

References 36 publications

Antitumor properties of Coenzyme Q0 against human ovarian carcinoma cells via induction of ROS-mediated apoptosis and cytoprotective autophagy

Antitumor properties of Coenzyme Q0 against human ovarian carcinoma cells via induction of ROS-mediated apoptosis and cytoprotective autophagy

Inhibition of Cronobacter Sakazakii Biofilm Formation and Expression of Virulence Factors by Coenzyme Q0

<i>In vitro </i>and <i>in vivo</i> toxicological assessments of <i>Antrodia cinnamomea</i> health food product (Leader <i>Antrodia cinnamomea</i> Capsule)

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