中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Specific N-glycan alterations are coupled in epithelial-mesenchymal transition induced by EGF in GE11 epithelial cells

文献类型:期刊论文

作者Xu, Qingsong1,2; Qu, Chen1; Wang, Wenjing3; Gu, Jianguo2; Du, Yuguang4; Song, Linsheng1
刊名CELL BIOLOGY INTERNATIONAL
出版日期2017-02-01
卷号41期号:2页码:124-133
ISSN号1065-6995
关键词bisecting GlcNAc epidermal growth factor epithelial-mesenchymal transition metastasis N-glycan tumorigenesis
英文摘要Epithelial-mesenchymal transition (EMT) is a phenomenon in cancer progression during which cancer cells undergo remarkable alteration acquiring highly invasive property. The aim of this study was to evaluate specific N-glycan alterations during EMT induced by epidermal growth factor (EGF) in GE11 epithelial cells. Herein, we demonstrated that EGF activated epidermal growth factor receptor (EGFR)/Akt/extracellular signal-regulated kinase (ERK) phosphorylation and promoted GE11 cell proliferation. Meanwhile, EGF stimulated the epithelial cells to undergo morphological alteration, destroying cell-cell inter-contact and exhibiting mesenchymal cells higher metastatic potential. A wound-healing assay showed the migratory ability increased 1.5-fold after EGF treatment. Moreover, the relative intensity of N-cadherin versus E-cadherin increased 2.6-fold, and the E-cadherin distribution in cell-cell junctions became jagged and faint after EGF incubation for 72h. Interestingly, the amounts of bisecting GlcNAc structure were dramatically declined, by contrast, the formation of 1,6 GlcNAc branches on cell surface was upregulated during EMT induced by EGF. To understand the roles of N-glycans in EGF-induced EMT, the cells were stably transfected with N-acetylglucosaminyltransferase III (GnT-III), which catalyzes the bisecting GlcNAc structure formation. As the markers for EMT, EGF-induced E-cadherin decrease and fibronectin increase were delayed in GnT-III-overexpressing cells. Taken together, these results demonstrated that specific N-glycan alterations were coupled in EMT induced by EGF, which might be contributed to diagnosis and therapy of tumor metastasis.
WOS标题词Science & Technology ; Life Sciences & Biomedicine
类目[WOS]Cell Biology
研究领域[WOS]Cell Biology
关键词[WOS]CANCER CELLS ; E-CADHERIN ; ACETYLGLUCOSAMINYLTRANSFERASE-III ; BREAST-CANCER ; GROWTH ; ACTIVATION ; METASTASIS ; MICROENVIRONMENT ; GLYCOSYLATION ; MORPHOGENESIS
收录类别SCI
语种英语
WOS记录号WOS:000393312200002
源URL[http://ir.ipe.ac.cn/handle/122111/21925]  
专题过程工程研究所_研究所(批量导入)
作者单位1.Dalian Ocean Univ, Coll Fisheries & Life Sci, Dalian 116023, Peoples R China
2.Tohoku Med & Pharmaceut Univ, Inst Mol Biomembrane & Glycobiol, Div Regulatory Glycobiol, Sendai, Miyagi 9818558, Japan
3.Dalian Elite Analyt Instruments Co Ltd, Dalian 116023, Peoples R China
4.Chinese Acad Sci, Inst Proc Engn, Beijing 100190, Peoples R China
推荐引用方式
GB/T 7714
Xu, Qingsong,Qu, Chen,Wang, Wenjing,et al. Specific N-glycan alterations are coupled in epithelial-mesenchymal transition induced by EGF in GE11 epithelial cells[J]. CELL BIOLOGY INTERNATIONAL,2017,41(2):124-133.
APA Xu, Qingsong,Qu, Chen,Wang, Wenjing,Gu, Jianguo,Du, Yuguang,&Song, Linsheng.(2017).Specific N-glycan alterations are coupled in epithelial-mesenchymal transition induced by EGF in GE11 epithelial cells.CELL BIOLOGY INTERNATIONAL,41(2),124-133.
MLA Xu, Qingsong,et al."Specific N-glycan alterations are coupled in epithelial-mesenchymal transition induced by EGF in GE11 epithelial cells".CELL BIOLOGY INTERNATIONAL 41.2(2017):124-133.

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来源:过程工程研究所

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