antroquinonol-d and Breast-Neoplasms

antroquinonol-d has been researched along with Breast-Neoplasms* in 2 studies

Other Studies

2 other study(ies) available for antroquinonol-d and Breast-Neoplasms

Article	Year
Hypermethylation of CCND2 in Lung and Breast Cancer Is a Potential Biomarker and Drug Target. International journal of molecular sciences, 2018, Oct-10, Volume: 19, Issue:10 Lung and breast cancer are the leading causes of mortality in women worldwide. The discovery of molecular alterations that underlie these two cancers and corresponding drugs has contributed to precision medicine. We found that CCND2 is a common target in lung and breast cancer. Hypermethylation of the Topics: Antineoplastic Agents; Biomarkers, Tumor; Breast Neoplasms; Cell Movement; Cell Proliferation; Cyclin D2; DNA Methylation; Dose-Response Relationship, Drug; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms; Prognosis; Promoter Regions, Genetic; Proportional Hazards Models; RNA, Messenger; Ubiquinone	2018
Antroquinonol from Antrodia Camphorata suppresses breast tumor migration/invasion through inhibiting ERK-AP-1- and AKT-NF-κB-dependent MMP-9 and epithelial-mesenchymal transition expressions. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2015, Volume: 78 Antroquinonol (ANQ) is an ubiquinon derivative isolated from the mycelium of Antrodia camphorata. However, the effect of ANQ on breast cancer treatment is unknown. We found that ANQ significantly suppressed the migration and invasion of breast cancer MDA-MB-231 cells, and inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced invasiveness by MCF7 cells. ANQ inhibiting MMP-9 gene expression and enzymatic activity occurred at transcriptional regulation. Mechanistically, activation of ERK and AKT is crucial for MMP-9 gene expression, and the addition of ANQ suppressed phosphorylation of ERK and AKT. The induction of the AP-1 and NF-κB pathway participated in MMP-9 gene expression. Suppression of ERK inhibited AP-1, whereas blocking AKT diminished NF-κB activity, and treatment with ANQ suppressed both AP-1 and NF-κB signaling. Moreover, ANQ suppressed EMT protein expression, and inhibited TPA-induced EMT through downregulating the ERK-AP-1 and AKT-NF-κB signaling cascades. Together, our data showed for the first time that ANQ inhibited breast cancer invasiveness by suppressing ERK-AP-1- and AKT-NF-κB-dependent MMP-9 and EMT expressions. Topics: Antrodia; Breast Neoplasms; Cell Line, Tumor; Cell Movement; Cell Survival; Down-Regulation; Epithelial-Mesenchymal Transition; Humans; Matrix Metalloproteinase 9; MCF-7 Cells; Mitogen-Activated Protein Kinase 3; NF-kappa B; Phosphorylation; Signal Transduction; Tetradecanoylphorbol Acetate; Transcription Factor AP-1; Ubiquinone	2015

Article

Year

Hypermethylation of CCND2 in Lung and Breast Cancer Is a Potential Biomarker and Drug Target.

International journal of molecular sciences, 2018, Oct-10, Volume: 19, Issue:10

Lung and breast cancer are the leading causes of mortality in women worldwide. The discovery of molecular alterations that underlie these two cancers and corresponding drugs has contributed to precision medicine. We found that CCND2 is a common target in lung and breast cancer. Hypermethylation of the

Topics: Antineoplastic Agents; Biomarkers, Tumor; Breast Neoplasms; Cell Movement; Cell Proliferation; Cyclin D2; DNA Methylation; Dose-Response Relationship, Drug; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms; Prognosis; Promoter Regions, Genetic; Proportional Hazards Models; RNA, Messenger; Ubiquinone

2018

Antroquinonol from Antrodia Camphorata suppresses breast tumor migration/invasion through inhibiting ERK-AP-1- and AKT-NF-κB-dependent MMP-9 and epithelial-mesenchymal transition expressions.

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2015, Volume: 78

Antroquinonol (ANQ) is an ubiquinon derivative isolated from the mycelium of Antrodia camphorata. However, the effect of ANQ on breast cancer treatment is unknown. We found that ANQ significantly suppressed the migration and invasion of breast cancer MDA-MB-231 cells, and inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced invasiveness by MCF7 cells. ANQ inhibiting MMP-9 gene expression and enzymatic activity occurred at transcriptional regulation. Mechanistically, activation of ERK and AKT is crucial for MMP-9 gene expression, and the addition of ANQ suppressed phosphorylation of ERK and AKT. The induction of the AP-1 and NF-κB pathway participated in MMP-9 gene expression. Suppression of ERK inhibited AP-1, whereas blocking AKT diminished NF-κB activity, and treatment with ANQ suppressed both AP-1 and NF-κB signaling. Moreover, ANQ suppressed EMT protein expression, and inhibited TPA-induced EMT through downregulating the ERK-AP-1 and AKT-NF-κB signaling cascades. Together, our data showed for the first time that ANQ inhibited breast cancer invasiveness by suppressing ERK-AP-1- and AKT-NF-κB-dependent MMP-9 and EMT expressions.

Topics: Antrodia; Breast Neoplasms; Cell Line, Tumor; Cell Movement; Cell Survival; Down-Regulation; Epithelial-Mesenchymal Transition; Humans; Matrix Metalloproteinase 9; MCF-7 Cells; Mitogen-Activated Protein Kinase 3; NF-kappa B; Phosphorylation; Signal Transduction; Tetradecanoylphorbol Acetate; Transcription Factor AP-1; Ubiquinone

2015