Epithelial Mesenchymal Transition in Embryonic Development, Tissue Repair and Cancer: A Comprehensive Overview

DOI Web Site 被引用文献2件
  • Do Kim
    Department of Anatomy and Cell Biology, East Carolina University, Greenville, NC 27834, USA
  • Tiaosi Xing
    Department of Anatomy and Cell Biology, East Carolina University, Greenville, NC 27834, USA
  • Zhibin Yang
    Department of Anatomy and Cell Biology, East Carolina University, Greenville, NC 27834, USA
  • Ronald Dudek
    Department of Anatomy and Cell Biology, East Carolina University, Greenville, NC 27834, USA
  • Qun Lu
    Department of Anatomy and Cell Biology, East Carolina University, Greenville, NC 27834, USA
  • Yan-Hua Chen
    Department of Anatomy and Cell Biology, East Carolina University, Greenville, NC 27834, USA

説明

<jats:p>The epithelial mesenchymal transition (EMT) plays a central role in both normal physiological events (e.g., embryonic development) and abnormal pathological events (e.g., tumor formation and metastasis). The processes that occur in embryonic development are often reactivated under pathological conditions such as oncogenesis. Therefore, defining the regulatory networks (both gene and protein levels) involved in the EMT during embryonic development will be fundamental in understanding the regulatory networks involved in tumor development, as well as metastasis. There are many molecules, factors, mediators and signaling pathways that are involved in the EMT process. Although the EMT is a very old topic with numerous publications, recent new technologies and discoveries give this research area some new perspective and direction. It is now clear that these important processes are controlled by a network of transcriptional and translational regulators in addition to post-transcriptional and post-translational modifications that amplify the initial signals. In this review article, we will discuss some key concepts, historical findings, as well as some recent progresses in the EMT research field.</jats:p>

収録刊行物

被引用文献 (2)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ