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Endothelin-1 promotes cell migration through epithelial-to-mesenchymal transition in human oral cancer
Biomarkers and Genomic Medicine (2014) 6, 189
Available online at www.sciencedirect.com
ScienceDirect journal homepage: www.j-bgm.com
ABSTRACT
Endothelin-1 promotes cell migration through epithelial-to-mesenchymal transition in human oral cancer Chia-Yun Huang a, Ching-Ping Wang b, Yi-Hao Chang b, Pei-Han Huang b, Chih-Hsin Tang c, Min-Huan Wu c,d,e a
Department of Biology Science of Technology, China Medical University, Taichung, Taiwan Department of Otolaryngology, Head and Neck Surgery, Taichung Veteran’s General Hospital, Taichung, Taiwan c Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan d Life Science Research Center, Tunghai University, Taichung, Taiwan e Physical Education Office, Tunghai University, Taichung, Taiwan b
Background: Oral cancer is one of the major causes of mortality in humans, and squamous cell carcinoma is the most common type of oral cancer. Endothelin-1 is known as a secretory protein presented in various types cells, which has been indicated as a factor for cancer pathology. The aim of the present study was to investigate the molecular mechanism of cell migration in oral cancer. Materials and Methods: ET-1-mediated matrix metalloproteinase N-cadherin and Twist expression was assessed by qPCR and Western blot analysis. The mechanisms of action of ET-1 in different signaling pathways were studied using Western blotting. Knockdown of proteins was achieved by transfection of siRNA. Results: Pretreatment of oral cancer cells (SCC4) with AMP-activated protein kinase (AMPKa) inhibitors or Twist siRNA abolished ET-1-promoted migration and increased the expression of N-cadherin. Besides, ET-1 demonstrably activated AMPKa and Twist signaling pathways. Furthermore, the expression levels of N-cadherin and Twist were correlated with human oral cancer specimens. Discussion: To sum up, our results indicate that ET-1 enhances the epithelial-to-mesenchymal transition (EMT) markers and migratory ability of human oral cancer cells by increasing N-cadherin expression via AMPKa and Twist pathways.
http://dx.doi.org/10.1016/j.bgm.2014.09.015 2214-0247/Copyright ª 2014, Taiwan Genomic Medicine and Biomarker Society. Published by Elsevier Taiwan LLC. All rights reserved.
Available online at www.sciencedirect.com
ScienceDirect journal homepage: www.j-bgm.com
ABSTRACT
Endothelin-1 promotes cell migration through epithelial-to-mesenchymal transition in human oral cancer Chia-Yun Huang a, Ching-Ping Wang b, Yi-Hao Chang b, Pei-Han Huang b, Chih-Hsin Tang c, Min-Huan Wu c,d,e a
Department of Biology Science of Technology, China Medical University, Taichung, Taiwan Department of Otolaryngology, Head and Neck Surgery, Taichung Veteran’s General Hospital, Taichung, Taiwan c Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan d Life Science Research Center, Tunghai University, Taichung, Taiwan e Physical Education Office, Tunghai University, Taichung, Taiwan b
Background: Oral cancer is one of the major causes of mortality in humans, and squamous cell carcinoma is the most common type of oral cancer. Endothelin-1 is known as a secretory protein presented in various types cells, which has been indicated as a factor for cancer pathology. The aim of the present study was to investigate the molecular mechanism of cell migration in oral cancer. Materials and Methods: ET-1-mediated matrix metalloproteinase N-cadherin and Twist expression was assessed by qPCR and Western blot analysis. The mechanisms of action of ET-1 in different signaling pathways were studied using Western blotting. Knockdown of proteins was achieved by transfection of siRNA. Results: Pretreatment of oral cancer cells (SCC4) with AMP-activated protein kinase (AMPKa) inhibitors or Twist siRNA abolished ET-1-promoted migration and increased the expression of N-cadherin. Besides, ET-1 demonstrably activated AMPKa and Twist signaling pathways. Furthermore, the expression levels of N-cadherin and Twist were correlated with human oral cancer specimens. Discussion: To sum up, our results indicate that ET-1 enhances the epithelial-to-mesenchymal transition (EMT) markers and migratory ability of human oral cancer cells by increasing N-cadherin expression via AMPKa and Twist pathways.
http://dx.doi.org/10.1016/j.bgm.2014.09.015 2214-0247/Copyright ª 2014, Taiwan Genomic Medicine and Biomarker Society. Published by Elsevier Taiwan LLC. All rights reserved.