期刊
EUROPEAN JOURNAL OF CANCER
卷 50, 期 2, 页码 366-378出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.ejca.2013.09.025
关键词
Epithelial-mesenchymal transition; Head and neck squamous cell carcinoma; TWIST1; Emodin
类别
资金
- National Science Council of the Republic of China [NSC100-2320-B-039-019, NSC101-2320-B-039-031-MY3]
- Department of Health (Taiwan)
- China Medical University Hospital Cancer Research Center of Excellence [DOH100-TD-C-111-005]
- China Medical University [CMU101-S-36]
Head and neck squamous cell carcinoma (HNSCC) is one of the leading causes of cancer deaths worldwide. In recent studies, a crucial link has been discovered between the acquisition of metastatic traits and tumour-initiating abilities in cancer cells during the epithelial-mesenchymal transition (EMT). Herein, we demonstrated that the ectopic expression of TWIST1, the EMT regulator, in HNSCC FaDu cells triggered EMT and resulted in the acquisition of a mesenchymal phenotype. Moreover, FaDu-pFLAG-TWIST1 cancer cell populations that were induced to EMT displayed an increased proportion of cells with the CD44 marker, which is associated with tumour initiation. Interestingly, we found that emodin treatment reduced the tumour-initiating abilities and inhibited cell migration and invasion in FaDu-pFLAG-TWIST1 cells. Emodin directly inhibited TWIST1 expression, upregulated E-cadherin mRNA and protein expression, and downregulated vimentin mRNA and protein expression. Moreover, we found that emodin inhibited TWIST1 binding to the E-cadherin promoter and repressed E-cadherin transcription activity. We also found that emodin inhibited TWIST1-induced EMT by inhibiting the beta-catenin and Akt pathways. More interestingly, emodin significantly inhibited TWIST1-induced invasion in vivo. Therefore, emodin might be applicable to anticancer therapy and could be a potential new therapeutic drug for HNSCC. (C) 2013 Elsevier Ltd. All rights reserved.
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