有哪些信誉好的足球投注网站a novel network integrating a mirna-203snai1 feedback loop which regulates epithelial to mesenchymal transition一种新颖的网络集成microrna - 203 snai1反馈回路调节上皮间充质转变.pdfVIP
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a novel network integrating a mirna-203snai1 feedback loop which regulates epithelial to mesenchymal transition一种新颖的网络集成microrna - 203 snai1反馈回路调节上皮间充质转变
A Novel Network Integrating a miRNA-203/SNAI1 Feedback Loop which Regulates Epithelial to Mesenchymal Transition ` 1 ´ 1 2 1 1 Michele Moes *, Antony Le Bechec , Isaac Crespo , Christina Laurini , Aliaksandr Halavatyi , 1 2 1 Guillaume Vetter , Antonio del Sol , Evelyne Friederich * 1 Cytoskeleton and Cell Plasticity Lab, Life Sciences Research Unit-FSCT, University of Luxembourg, Luxembourg, Luxembourg, 2 Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg Abstract Background: The majority of human cancer deaths are caused by metastasis. The metastatic dissemination is initiated by the breakdown of epithelial cell homeostasis. During this phenomenon, referred to as epithelial to mesenchymal transition (EMT), cells change their genetic and trancriptomic program leading to phenotypic and functional alterations. The challenge of understanding this dynamic process resides in unraveling regulatory networks involving master transcription factors (e.g. SNAI1/2, ZEB1/2 and TWIST1) and microRNAs. Here we investigated microRNAs regulated by SNAI1 and their potential role in the regulatory networks underlying epithelial plasticity. Results: By a large-scale analysis on epithelial plasticity, we highlighted miR-203 and its molecular link with SNAI1 and the miR-200 family, key regulators of epithelial homeostasis. During SNAI1-induced EMT in MCF7 breast cancer cells, miR-203 and miR-200 family members were repressed in a timely correlated manner. Importantly, miR-203 repressed endogenous SNAI1, forming a double negative miR203/SNAI1 feedback loop. We integrated this novel miR203/SNAI1 with the known miR200/ZEB feedba
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