DICP OpenIR
学科主题生物化学
Roles of N-acetylglucosaminyltransferase III in Epithelial-to-mesenchymal Transition Induced by TGF-β1
Xu QS(许青松); Gu JG(顾建国); Du YG(杜昱光); YuguangDu
会议文集Asian Communications of Glycobiology and Glycotechnology
会议名称The 3rd Asian Communications of Glycobiology and Glycotechnology
会议日期2011-10-27
2011
会议地点上海
其他题名N-乙酰氨基葡萄糖转移酶III在转化生长因子β1诱导的上皮间质转化中的作用
页码71-0
出版者待补充
出版地待补充
合作性质墙报
部门归属1805
主办者中国科学院上海有机化学所
英文摘要The epithelial-to-mesenchymal transition (EMT) plays crucial roles in the embryonic development, wound healing, tissue repair and cancer progression. In the present study, we demonstrate that transforming growth factor β (TGF-β) down-regulated expression of N-acetylglucosaminyltransferase III (GnT-III) during EMT. The treatment with TGF-β1 resulted in a decrease in E-cadherin expression and GnT-III expression as well as its product, the bisected N-glycans, which was confirmed by E4-PHA lectin blot in human MCF-10A and mouse GE11 cells. To understand roles of GnT-III expression in EMT, the MCF-10A cell was stably transfected with GnT-III. Of particular interesting, overexpression of GnT-III partially, but did inhibit EMT induced by TGF-β1, which were confirmed by cell morphological changes of phase-contrast, immunochemical staining patterns of E-cadherin and actin. In addition, GnT-III modified E-cadherin, which contributed to prolong E-cadherin turnover on cell surface examined by biotinylation and pulse-chase experiments. Consistently, GnT-III expression inhibited β-catenin translocation from cell-cell contact into cytoplasm and nucleus. Furthermore, the transwell assay showed that GnT-III expression suppresses TGF-β-induced cell motility. Taken together, these observations are the first to clearly demonstrate that GnT-III plays important roles in EMT, and explain a molecular mechanism for inhibitory effects of GnT-III on cancer metastasis.; The epithelial-to-mesenchymal transition (EMT) plays crucial roles in the embryonic development, wound healing, tissue repair and cancer progression. In the present study, we demonstrate that transforming growth factor β (TGF-β) down-regulated expression of N-acetylglucosaminyltransferase III (GnT-III) during EMT. The treatment with TGF-β1 resulted in a decrease in E-cadherin expression and GnT-III expression as well as its product, the bisected N-glycans, which was confirmed by E4-PHA lectin blot in human MCF-10A and mouse GE11 cells. To understand roles of GnT-III expression in EMT, the MCF-10A cell was stably transfected with GnT-III. Of particular interesting, overexpression of GnT-III partially, but did inhibit EMT induced by TGF-β1, which were confirmed by cell morphological changes of phase-contrast, immunochemical staining patterns of E-cadherin and actin. In addition, GnT-III modified E-cadherin, which contributed to prolong E-cadherin turnover on cell surface examined by biotinylation and pulse-chase experiments. Consistently, GnT-III expression inhibited β-catenin translocation from cell-cell contact into cytoplasm and nucleus. Furthermore, the transwell assay showed that GnT-III expression suppresses TGF-β-induced cell motility. Taken together, these observations are the first to clearly demonstrate that GnT-III plays important roles in EMT, and explain a molecular mechanism for inhibitory effects of GnT-III on cancer metastasis.
文献类型会议论文
条目标识符http://cas-ir.dicp.ac.cn/handle/321008/116087
专题中国科学院大连化学物理研究所
通讯作者YuguangDu
推荐引用方式
GB/T 7714
Xu QS,Gu JG,Du YG,et al. Roles of N-acetylglucosaminyltransferase III in Epithelial-to-mesenchymal Transition Induced by TGF-β1[C]. 待补充:待补充,2011:71-0.
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