Antrodin C Inhibits Epithelial-to-Mesenchymal Transition and Metastasis of Breast Cancer Cells via Suppression of Smad2/3 and β-Catenin Signaling Pathways

Epithelial-to-mesenchymal transition (EMT) is a crucial event involved metastasis of certain tumors. Thus, identifying chemical agents that can block EMT is highly warranted for the development of anti-cancer chemoprevention/chemotherapies. In this study, we found that Antrodin C (ADC), a maleimide...

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Published inPloS one Vol. 10; no. 2; p. e0117111
Main Authors Kumar, K. J. Senthil, Vani, M. Gokila, Chueh, Pin-Ju, Mau, Jeng-Leun, Wang, Sheng-Yang
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 06.02.2015
Public Library of Science (PLoS)
Subjects
Actin
Actin Cytoskeleton - drug effects
Actin Cytoskeleton - metabolism
Agricultural biotechnology
Antineoplastic Agents - chemistry
Antineoplastic Agents - isolation & purification
Antineoplastic Agents - pharmacology
Antrodia - chemistry
Antrodia - metabolism
Antrodia cinnamomea
Breast cancer
Breast carcinoma
Breast Neoplasms - metabolism
Breast Neoplasms - pathology
Cadherins - metabolism
Cancer
Cell adhesion & migration
Cell Movement - drug effects
Cell Survival - drug effects
Chemical agents
Chemotherapy
Cytoskeleton
Down-Regulation - drug effects
E-cadherin
Epithelial-Mesenchymal Transition - drug effects
Extracellular matrix
Female
Food
Food production
Gelatinase A
Humans
Insulin-like growth factors
Kinases
Maleimides - chemistry
Maleimides - isolation & purification
Maleimides - pharmacology
Markers
Matrix Metalloproteinase 2 - metabolism
Matrix Metalloproteinase 9 - metabolism
MCF-7 Cells
Mesenchyme
Metastases
Metastasis
N-Cadherin
Natural & organic foods
R&D
Regulators
Research & development
Signal transduction
Signal Transduction - drug effects
Signaling
Smad protein
Smad2 protein
Smad2 Protein - metabolism
Smad3 protein
Smad3 Protein - metabolism
Transforming Growth Factor beta1 - pharmacology
Transforming growth factor-b1
Tumors
U-Plasminogen activator
Up-Regulation - drug effects
Urokinase
Vimentin
Womens health
β-Catenin
United States > US
Taiwan
California
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Abstract Epithelial-to-mesenchymal transition (EMT) is a crucial event involved metastasis of certain tumors. Thus, identifying chemical agents that can block EMT is highly warranted for the development of anti-cancer chemoprevention/chemotherapies. In this study, we found that Antrodin C (ADC), a maleimide derivative isolated from Antrodia cinnamomea health food product inhibits TGF-β1-induced EMT and breast cancer cell metastasis in vitro. Pretreatment of MCF-7 cells with ADC significantly blocked TGF-β1-induced phenotypic changes and actin cytoskeleton remodeling. In addition, ADC was able to up-regulate epithelial markers such as E-cadherin and occludin, whereas mesenchymal markers including N-cadherin and vimentin were significantly inhibited, possibly through the modulation of transcriptional regulators Smad/Smad3. ADC blocked TGF-β1-induced migration and invasion of MCF-7 cells through the down-regulation of matrix-metalloproteinases (MMP-2, -9) and urokinase plasminogen activator (uPA). The inhibition of MMPs and uPA activity by ADC was reasoned by suppression of its corresponding transcription factor β-catenin. Taken together, our data suggested that ADC attenuates the TGF-β1-induced EMT, migration and invasion of human breast carcinoma through the suppression of Smad2/3 and β-catenin signaling pathways.
AbstractList Epithelial-to-mesenchymal transition (EMT) is a crucial event involved metastasis of certain tumors. Thus, identifying chemical agents that can block EMT is highly warranted for the development of anti-cancer chemoprevention/chemotherapies. In this study, we found that Antrodin C (ADC), a maleimide derivative isolated from Antrodia cinnamomea health food product inhibits TGF-β1-induced EMT and breast cancer cell metastasis in vitro. Pretreatment of MCF-7 cells with ADC significantly blocked TGF-β1-induced phenotypic changes and actin cytoskeleton remodeling. In addition, ADC was able to up-regulate epithelial markers such as E-cadherin and occludin, whereas mesenchymal markers including N-cadherin and vimentin were significantly inhibited, possibly through the modulation of transcriptional regulators Smad/Smad3. ADC blocked TGF-β1-induced migration and invasion of MCF-7 cells through the down-regulation of matrix-metalloproteinases (MMP-2, -9) and urokinase plasminogen activator (uPA). The inhibition of MMPs and uPA activity by ADC was reasoned by suppression of its corresponding transcription factor β-catenin. Taken together, our data suggested that ADC attenuates the TGF-β1-induced EMT, migration and invasion of human breast carcinoma through the suppression of Smad2/3 and β-catenin signaling pathways.Epithelial-to-mesenchymal transition (EMT) is a crucial event involved metastasis of certain tumors. Thus, identifying chemical agents that can block EMT is highly warranted for the development of anti-cancer chemoprevention/chemotherapies. In this study, we found that Antrodin C (ADC), a maleimide derivative isolated from Antrodia cinnamomea health food product inhibits TGF-β1-induced EMT and breast cancer cell metastasis in vitro. Pretreatment of MCF-7 cells with ADC significantly blocked TGF-β1-induced phenotypic changes and actin cytoskeleton remodeling. In addition, ADC was able to up-regulate epithelial markers such as E-cadherin and occludin, whereas mesenchymal markers including N-cadherin and vimentin were significantly inhibited, possibly through the modulation of transcriptional regulators Smad/Smad3. ADC blocked TGF-β1-induced migration and invasion of MCF-7 cells through the down-regulation of matrix-metalloproteinases (MMP-2, -9) and urokinase plasminogen activator (uPA). The inhibition of MMPs and uPA activity by ADC was reasoned by suppression of its corresponding transcription factor β-catenin. Taken together, our data suggested that ADC attenuates the TGF-β1-induced EMT, migration and invasion of human breast carcinoma through the suppression of Smad2/3 and β-catenin signaling pathways.
Epithelial-to-mesenchymal transition (EMT) is a crucial event involved metastasis of certain tumors. Thus, identifying chemical agents that can block EMT is highly warranted for the development of anti-cancer chemoprevention/chemotherapies. In this study, we found that Antrodin C (ADC), a maleimide derivative isolated from Antrodia cinnamomea health food product inhibits TGF-β1-induced EMT and breast cancer cell metastasis in vitro. Pretreatment of MCF-7 cells with ADC significantly blocked TGF-β1-induced phenotypic changes and actin cytoskeleton remodeling. In addition, ADC was able to up-regulate epithelial markers such as E-cadherin and occludin, whereas mesenchymal markers including N-cadherin and vimentin were significantly inhibited, possibly through the modulation of transcriptional regulators Smad/Smad3. ADC blocked TGF-β1-induced migration and invasion of MCF-7 cells through the down-regulation of matrix-metalloproteinases (MMP-2, -9) and urokinase plasminogen activator (uPA). The inhibition of MMPs and uPA activity by ADC was reasoned by suppression of its corresponding transcription factor β-catenin. Taken together, our data suggested that ADC attenuates the TGF-β1-induced EMT, migration and invasion of human breast carcinoma through the suppression of Smad2/3 and β-catenin signaling pathways.
Epithelial-to-mesenchymal transition (EMT) is a crucial event involved metastasis of certain tumors. Thus, identifying chemical agents that can block EMT is highly warranted for the development of anti-cancer chemoprevention/chemotherapies. In this study, we found that Antrodin C (ADC), a maleimide derivative isolated from Antrodia cinnamomea health food product inhibits TGF-β1-induced EMT and breast cancer cell metastasis in vitro . Pretreatment of MCF-7 cells with ADC significantly blocked TGF-β1-induced phenotypic changes and actin cytoskeleton remodeling. In addition, ADC was able to up-regulate epithelial markers such as E-cadherin and occludin, whereas mesenchymal markers including N-cadherin and vimentin were significantly inhibited, possibly through the modulation of transcriptional regulators Smad/Smad3. ADC blocked TGF-β1-induced migration and invasion of MCF-7 cells through the down-regulation of matrix-metalloproteinases (MMP-2, -9) and urokinase plasminogen activator (uPA). The inhibition of MMPs and uPA activity by ADC was reasoned by suppression of its corresponding transcription factor β-catenin. Taken together, our data suggested that ADC attenuates the TGF-β1-induced EMT, migration and invasion of human breast carcinoma through the suppression of Smad2/3 and β-catenin signaling pathways.
Author Mau, Jeng-Leun
Chueh, Pin-Ju
Wang, Sheng-Yang
Vani, M. Gokila
Kumar, K. J. Senthil
AuthorAffiliation 5 National Chung Hsing University/University of California at Davis, Plant and Food Biotechnology Center, National Chung Hsing University, Taichung, Taiwan
3 Department of Biotechnology, Asia University, Taichung, Taiwan
1 Department of Forestry, National Chung Hsing University, Taichung, Taiwan
2 Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan
The University of Hong Kong, CHINA
4 Department of Food Science and Biotechnology, National Chung Hsing University, Taichung, Taiwan
6 Agricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan
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These authors contributed equally to this work.
Competing Interests: The authors have declared that no competing interests exist.
Conceived and designed the experiments: SYW. Performed the experiments: MGV KJSK. Analyzed the data: KJSK MGV PJC JLM. Wrote the paper: KJSK MGV PJC SYW.
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Snippet Epithelial-to-mesenchymal transition (EMT) is a crucial event involved metastasis of certain tumors. Thus, identifying chemical agents that can block EMT is...
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StartPage e0117111
SubjectTerms Actin
Actin Cytoskeleton - drug effects
Actin Cytoskeleton - metabolism
Agricultural biotechnology
Antineoplastic Agents - chemistry
Antineoplastic Agents - isolation & purification
Antineoplastic Agents - pharmacology
Antrodia - chemistry
Antrodia - metabolism
Antrodia cinnamomea
Breast cancer
Breast carcinoma
Breast Neoplasms - metabolism
Breast Neoplasms - pathology
Cadherins - metabolism
Cancer
Cell adhesion & migration
Cell Movement - drug effects
Cell Survival - drug effects
Chemical agents
Chemotherapy
Cytoskeleton
Down-Regulation - drug effects
E-cadherin
Epithelial-Mesenchymal Transition - drug effects
Extracellular matrix
Female
Food
Food production
Gelatinase A
Humans
Insulin-like growth factors
Kinases
Maleimides - chemistry
Maleimides - isolation & purification
Maleimides - pharmacology
Markers
Matrix Metalloproteinase 2 - metabolism
Matrix Metalloproteinase 9 - metabolism
MCF-7 Cells
Mesenchyme
Metastases
Metastasis
N-Cadherin
Natural & organic foods
R&D
Regulators
Research & development
Signal transduction
Signal Transduction - drug effects
Signaling
Smad protein
Smad2 protein
Smad2 Protein - metabolism
Smad3 protein
Smad3 Protein - metabolism
Transforming Growth Factor beta1 - pharmacology
Transforming growth factor-b1
Tumors
U-Plasminogen activator
Up-Regulation - drug effects
Urokinase
Vimentin
Womens health
β-Catenin
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Title Antrodin C Inhibits Epithelial-to-Mesenchymal Transition and Metastasis of Breast Cancer Cells via Suppression of Smad2/3 and β-Catenin Signaling Pathways
URI https://www.ncbi.nlm.nih.gov/pubmed/25658913
https://www.proquest.com/docview/1656719365
https://www.proquest.com/docview/1653127570
https://pubmed.ncbi.nlm.nih.gov/PMC4319743
https://doaj.org/article/e3ae2576e31d42e2861912b52784059d
http://dx.doi.org/10.1371/journal.pone.0117111
Volume 10
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