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题名: Roles of N-Acetylglucosaminyltransferase III in Epithelial-to-Mesenchymal Transition Induced by Transforming Growth Factor beta 1 (TGF-beta 1) in Epithelial Cell Lines
作者: Xu, Qingsong1, 2;  Isaji, Tomoya1;  Lu, Yingying1;  Gu, Wei1;  Kondo, Madoka1;  Fukuda, Tomohiko1;  Du, Yuguang2;  Gu, Jianguo1
刊名: JOURNAL OF BIOLOGICAL CHEMISTRY
发表日期: 2012-05-11
DOI: 10.1074/jbc.M111.262154
卷: 287, 期:20, 页:16563-16574
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology ;  Life Sciences & Biomedicine
类目[WOS]: Biochemistry & Molecular Biology
研究领域[WOS]: Biochemistry & Molecular Biology
英文摘要: The epithelial-to-mesenchymal transition (EMT) plays crucial roles in embryonic development, wound healing, tissue repair, and cancer progression. Results of this study show how transforming growth factor beta 1 (TGF-beta 1) down-regulates expression of N-acetylglucosaminyltransferase III (GnT-III) during EMT-like changes. Treatment with TGF-beta 1 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 erythro-agglutinating phytohemagglutinin lectin blot and HPLC analysis in human MCF-10A and mouse GE11 cells. In contrast with GnT-III, the expression of N-acetylglucosaminyltransferase V was slightly enhanced by TGF-beta 1 treatment. Changes in the N-glycan patterns on alpha 3 beta 1 integrin, one of the target proteins for GnT-III, were also confirmed by lectin blot analysis. To understand the roles of GnT-III expression in EMT-like changes, the MCF-10A cell was stably transfected with GnT-III. It is of particular interest that overexpression of GnT-III influenced EMT-like changes induced by TGF-beta 1, which was confirmed by cell morphological changes of phase contrast, immunochemical staining patterns of E-cadherin, and actin. In addition, GnT-III modified E-cadherin, which served to prolong E-cadherin turnover on the cell surface examined by biotinylation and pulse-chase experiments. GnT-III expression consistently inhibited beta-catenin translocation from cell-cell contact into the cytoplasm and nucleus. Furthermore, the transwell assay showed that GnT-III expression suppressed TGF-beta 1-induced cell motility. Taken together, these observations are the first to clearly demonstrate that GnT-III affects cell properties, which in turn influence EMT-like changes, and to explain a molecular mechanism for the inhibitory effects of GnT-III on cancer metastasis.
关键词[WOS]: E-CADHERIN ;  GLYCOSYLATION AFFECTS ;  TUMOR PROGRESSION ;  BREAST-CARCINOMA ;  PROPELLER DOMAIN ;  BISECTING GLCNAC ;  MOUSE MELANOMA ;  EXPRESSION ;  ADHESION ;  CATENIN
语种: 英语
WOS记录号: WOS:000304030900046
Citation statistics: 
内容类型: 期刊论文
URI标识: http://cas-ir.dicp.ac.cn/handle/321008/138064
Appears in Collections:中国科学院大连化学物理研究所_期刊论文

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作者单位: 1.Tohoku Pharmaceut Univ, Inst Mol Biomembrane & Glycobiol, Div Regulatory Glycobiol, Aoba Ku, Sendai, Miyagi 9818558, Japan
2.Chinese Acad Sci, Dalian Inst Chem Phys, Dalian 116023, Peoples R China

Recommended Citation:
Xu, Qingsong,Isaji, Tomoya,Lu, Yingying,et al. Roles of N-Acetylglucosaminyltransferase III in Epithelial-to-Mesenchymal Transition Induced by Transforming Growth Factor beta 1 (TGF-beta 1) in Epithelial Cell Lines[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2012,287(20):16563-16574.
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