Multiple Molecular Targets of Antrodia camphorata: A Suitable Candidate for Breast Cancer Chemoprevention

Yang, Hsin‐Ling; Kumar, K. J. Senthil; Hseu, You‐Cheng

doi:10.5772/21789

Cited by 6 publications

(18 citation statements)

References 65 publications

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“…Antrodia camphorata (AC) is well known in Taiwan as a physiologically beneficial mushroom. There is increasing evidence that AC possesses an extensive range of biological activities, including antioxidant, hepatoprotective, anti-hypertensive, anti-hyperlipidemic, immunomodulatory, and anti-inflammatory properties [ 29 , 30 ]. AC also exerted potent anti-cancer activity against a variety of cancer cells, including breast, liver, bladder, prostate, oral, colon, lung, pancreatic and leukemic cells [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

“…There is increasing evidence that AC possesses an extensive range of biological activities, including antioxidant, hepatoprotective, anti-hypertensive, anti-hyperlipidemic, immunomodulatory, and anti-inflammatory properties [ 29 , 30 ]. AC also exerted potent anti-cancer activity against a variety of cancer cells, including breast, liver, bladder, prostate, oral, colon, lung, pancreatic and leukemic cells [ 30 ]. The inhibitory effect against cancer cells by AC may be mediated by various cellular mechanisms of actions, such as regulation of oncogene and tumor suppressor gene expression, inhibition of metastasis and angiogenesis regulatory proteins, down-regulation of signal transduction pathways involving NF-κB, AP-1, Nrf2, and MAPK, induction of cell-cycle arrest, and apoptosis involving the Wnt/β-catenin, p53, death ligands, Bcl-2 and caspase families [ 23 , 29 , 30 ].…”

Section: Discussionmentioning

confidence: 99%

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In vitro and in vivo anti-tumor activity of CoQ0 against melanoma cells: inhibition of metastasis and induction of cell-cycle arrest and apoptosis through modulation of Wnt/β-catenin signaling pathways

et al. 2016

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Coenzyme Q0 (CoQ0, 2,3-dimethoxy-5-methyl-1,4-benzoquinone), a novel quinone derivative, has been shown to modulate cellular redox balance. However, effect of this compound on melanoma remains unclear. This study examined the in vitro or in vivo anti-tumor, apoptosis, and anti-metastasis activities of CoQ0 (0-20 μM) through inhibition of Wnt/β-catenin signaling pathway. CoQ0 exhibits a significant cytotoxic effect on melanoma cell lines (B16F10, B16F1, and A2058), while causing little toxicity toward normal (HaCaT) cells. The suppression of β-catenin was seen with CoQ0 administration accompanied by a decrease in the expression of Wnt/β-catenin transcriptional target c-myc, cyclin D1, and survivin through GSK3β-independent pathway. We found that CoQ0 treatment caused G1 cell-cycle arrest by reducing the levels of cyclin E and CDK4. Furthermore, CoQ0 treatment induced apoptosis through caspase-9/-3 activation, PARP degradation, Bcl-2/Bax dysregulation, and p53 expression. Notably, non- or sub-cytotoxic concentrations of CoQ0 markedly inhibited migration and invasion, accompanied by the down-regulation of MMP-2 and -9, and up-regulation of TIMP-1 and -2 expressions in highly metastatic B16F10 cells. Furthermore, the in vivo study results revealed that CoQ0 treatment inhibited the tumor growth in B16F10 xenografted nude mice. Histological analysis and western blotting confirmed that CoQ0 significantly decreased the xenografted tumor progression as demonstrated by induction of apoptosis, suppression of β-catenin, and inhibition of cell cycle-, apoptotic-, and metastatic-regulatory proteins. The data suggest that CoQ0 unveils a novel mechanism by down-regulating Wnt/β-catenin pathways and could be used as a potential lead compound for melanoma chemotherapy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

In vitro and in vivo anti-tumor activity of CoQ0 against melanoma cells: inhibition of metastasis and induction of cell-cycle arrest and apoptosis through modulation of Wnt/β-catenin signaling pathways

et al. 2016

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“…This study demonstrated for the first time that Antrodia camphorata exhibits potent antiplatelet activity via inhibiting both PKC and Akt activation in washed human platelets ( Figure 4(b) ). Antrodia camphorata has been used in traditional Chinese medicine to treat food poisoning, drug intoxication, diarrhea, abdominal pain, hypertension, skin irritation, and cancer [ 2 ]. Recent studies have reported that Antrodia camphorata induces substantial apoptosis in human promyelocytic leukemia (HL-60) cells [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

“…Antrodia camphorata is a rare Taiwanese medicinal mushroom that is popularly known as “niu cheng zhi” in Taiwan [ 1 ]. Antrodia camphorata has been used in traditional Chinese medicine to treat food poisoning, drug intoxication, diarrhea, abdominal pain, hypertension, skin irritation, and cancer [ 2 ]. Studies have identified bioactive compounds of Antrodia camphorata , including polysaccharides, maleic/succinic acid derivatives, triterpenoids, benzenoids, and benzoquinone derivatives [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

Effect ofAntrodiacamphorataon Inflammatory Arterial Thrombosis-Mediated Platelet Activation: The Pivotal Role of Protein Kinase C

Lin

Lan³

et al. 2014

The Scientific World Journal

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Antrodia camphorata is a rare Taiwanese medicinal mushroom. Antrodia camphorata extract has been reported to exhibit antioxidant, anti-inflammation, antimetastasis, and anticancer activities and plays a role in liver fibrosis, vasorelaxation, and immunomodulation. Critical vascular inflammation leads to vascular dysfunction and cardiovascular diseases, including abdominal aortic aneurysms, hypertension, and atherosclerosis. Platelet activation plays a crucial role in intravascular thrombosis, which is involved in a wide variety of cardiovascular diseases. However, the effect of Antrodia camphorata on platelet activation remains unclear. We examined the effects of Antrodia camphorata on platelet activation. In the present study, Antrodia camphorata treatment (56–224 μg/mL) inhibited platelet aggregation induced by collagen, but not U46619, an analogue of thromboxane A2, thrombin, and arachidonic acid. Antrodia camphorata inhibited collagen-induced calcium (Ca2+) mobilization and phosphorylation of protein kinase C (PKC) and Akt. In addition, Antrodia camphorata significantly reduced the aggregation and phosphorylation of PKC in phorbol-12, 13-dibutyrate (PDBu) activated platelets. In conclusion, Antrodia camphorata may inhibit platelet activation by inhibiting of Ca2+ and PKC cascade and the Akt pathway. Our study suggests that Antrodia camphorata may be a potential therapeutic agent for preventing or treating thromboembolic disorders.

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“…The inhibitory effect against cancer cells by Antrodia camphorata could be mediated by different cellular mechanisms of actions, such as inhibition of metastasis and angiogenesis regulatory proteins; regulation of oncogene and tumor suppressor gene expression; downregulation of signal transduction cascades involving Nrf2, NF-κB, AP-1, and MAPK; induction of cell-cycle arrest; and apoptosis involving the Wnt/β-catenin, p53, death ligands, Bcl-2, and caspase families. 11 , 13 , 14 According to our previous results of high-performance liquid chromatography analysis, the amount of CoQ 0 in the fermented culture broth of Antrodia camphorata was 17.3% (254 nm). 15 …”

Section: Introductionmentioning

confidence: 92%

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

et al. 2016

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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.

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Multiple Molecular Targets of Antrodia camphorata: A Suitable Candidate for Breast Cancer Chemoprevention

Cited by 6 publications

References 65 publications

In vitro and in vivo anti-tumor activity of CoQ0 against melanoma cells: inhibition of metastasis and induction of cell-cycle arrest and apoptosis through modulation of Wnt/β-catenin signaling pathways

In vitro and in vivo anti-tumor activity of CoQ0 against melanoma cells: inhibition of metastasis and induction of cell-cycle arrest and apoptosis through modulation of Wnt/β-catenin signaling pathways

Effect ofAntrodiacamphorataon Inflammatory Arterial Thrombosis-Mediated Platelet Activation: The Pivotal Role of Protein Kinase C

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

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Multiple Molecular Targets of Antrodia camphorata: A Suitable Candidate for Breast Cancer Chemoprevention

Cited by 6 publications

References 65 publications

In vitro and in vivo anti-tumor activity of CoQ0 against melanoma cells: inhibition of metastasis and induction of cell-cycle arrest and apoptosis through modulation of Wnt/β-catenin signaling pathways

In vitro and in vivo anti-tumor activity of CoQ0 against melanoma cells: inhibition of metastasis and induction of cell-cycle arrest and apoptosis through modulation of Wnt/β-catenin signaling pathways

Effect ofAntrodiacamphorataon Inflammatory Arterial Thrombosis-Mediated Platelet Activation: The Pivotal Role of Protein Kinase C

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

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