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題 名 | Epigenetic Regulation of Epithelial-mesenchymal Transition: Focusing on Hypoxia and TGF-β Signaling |
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作 者 | Lin, Yueh-te; Wu, Kou-juey; | 書刊名 | Journal of Biomedical Science |
卷 期 | 27 2020[民109] |
頁 次 | 頁(39)1-(39)10 |
分類號 | 410.1636 |
關鍵詞 | Epithelial-mesenchymal transition; Hypoxia; TGF-β; Epigenetic regulation; HIF-1α; HDAC3; WDR5; H3K4Ac; ChIP; LSD1; H2A.Z; |
語 文 | 英文(English) |
DOI | 10.1186/s12929-020-00632-3 |
英文摘要 | Epithelial-mesenchymal transition (EMT) is an important process triggered during cancer metastasis. Regulation of EMT is mostly initiated by outside signalling, including TGF-β, growth factors, Notch ligand, Wnt, and hypoxia. Many signalling pathways have been delineated to explain the molecular mechanisms of EMT. In this review, we will focus on the epigenetic regulation of two critical EMT signalling pathways: hypoxia and TGF-β. For hypoxia, hypoxia-induced EMT is mediated by the interplay between chromatin modifiers histone deacetylase 3 (HDAC3) and WDR5 coupled with the presence of histone 3 lysine 4 acetylation (H3K4Ac) mark that labels the promoter regions of various traditional EMT marker genes (e.g. CDH1, VIM). Recently identified new hypoxia-induced EMT markers belong to transcription factors (e.g. SMO, GLI1) that mediate EMT themselves. For TGF-β-induced ΕΜΤ, global chromatin changes, removal of a histone variant (H2A.Z), and new chromatin modifiers (e.g. UTX, Rad21, PRMT5, RbBP5, etc) are identified to be crucial for the regulation of both EMT transcription factors (EMT-TFs) and EMT markers (EMT-Ms). The epigenetic mechanisms utilized in these two pathways may serve as good model systems for other signalling pathways and also provide new potential therapeutic targets. |
本系統中英文摘要資訊取自各篇刊載內容。