ASIA unversity:Item 310904400/79679
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    题名: Emodin represses TWIST1-induced epithelial-mesenchymal transition in head and neck squamous cell carcinoma cells through the inhibition of β-catenin and Akt pathways
    作者: Tzong-Der Way;Jhen-Ting Huang;Chun-Hung Chou;Chi-Hung Huang;Muh-Hwa Yang;Chi-Tang Hog
    贡献者: 保健營養生技學系
    关键词: Epithelial–mesenchymal transition;Head and neck squamous cell carcinoma;TWIST1;Emodin
    日期: 2014-01
    上传时间: 2014-06-05 03:51:56 (UTC+0)
    摘要: 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 β-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.
    關聯: EUROPEAN JOURNAL OF CANCER,50(2),366–378.
    显示于类别:[國際企業學系] 期刊論文

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