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In the present study, we found that N-acetylglucosaminyltransferase I (GnT-I), an important enzyme in N-glycosylation, works as a switch to turn on/off the epithelial-to-mesenchymal transition (EMT), which plays crucial roles in not only physiological processes such as embryogenesis and organ development, but also tissue repair and pathological processes such as tissue fibrosis, tumor invasiveness, and metastasis. A deletion of GnT-I suppressed EMT and induced MET, a reversible process of EMT. Furthermore, a restoration of GnT-I in the GnT-I deficient cells rescued EMT phenotypes. EMT has been indicated to be involved in acquiring drug resistance. Here, we also showed the expression of GnT-I was important for cell survival, resistance to cancer drugs. Considering initiation of metastasis requires invasion, which is enabled by EMT, we believe that GnT-I is a promising cancer therapeutic target._x000D_ So far, the most of studies on EMT are mainly focused on some specific transcription factors at transcriptional levels. This study clearly suggested that posttranscriptional modification, N-glycosylation, also plays very important roles in EMT as well as cancer metastasis.

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This page is a summary of: N-acetylglucosaminyltransferase-I as a novel regulator of epithelial-mesenchymal transition, The FASEB Journal, February 2019, Federation of American Societies For Experimental Biology (FASEB),
DOI: 10.1096/fj.201801478r.
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