期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 486, 期 1, 页码 64-72出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2009.02.005
关键词
N-acetylglucosaminyltransferase-V; Receptor protein tyrosine phosphatase; kappa; EGFR; FAK; ERK; Furin; Swainsonine; Phosphatase; Phosphorylation; Cell migration
资金
- Shanghai Leading Academic Discipline Project [13110]
- National Natural Science Foundation of China [30670468]
N-acetylglucosaminyltransferase-V (GnT-V) has been reported to be closely associated with tumor migration, but the mechanism has been not currently clear. In this study we found that GnT-V activated EGFR signaling and promoted cell migration through receptor protein tyrosine phosphatase kappa (RPTP kappa). The overexpression of GnT-V gene in human hepatoma SMMC-7721 cell line not only induced the addition of beta 1,6 GlcNAc branch to N-glycan of RPTP kappa but also decreased the protein level of RPTP kappa, which both contributed to the decreased phosphatase activity of RPTP kappa activating subsequently EGFR signaling. Moreover, we found that the knockdown of RPTP kappa and its addition of PI,6 GlcNAc branch both promoted cell migration, which could be ascribed to the activation of EGFR signaling regulated by RPTP kappa. Therefore, our findings could provide an insight into the molecular mechanism of how GnT-V promoted cell migration, suggesting that RPTP kappa could be one of factors regulating the EGF-mediated migration signals. (C) 2009 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据