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Specific N-glycan alterations are coupled in epithelial-mesenchymal transition induced by EGF in GE11 epithelial cells
Xu, Qingsong1,2; Qu, Chen1; Wang, Wenjing3; Gu, Jianguo2; Du, Yuguang4; Song, Linsheng1
2017-02-01
Source PublicationCELL BIOLOGY INTERNATIONAL
ISSN1065-6995
Volume41Issue:2Pages:124-133
Abstract

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.

KeywordBisecting Glcnac Epidermal Growth Factor Epithelial-mesenchymal Transition Metastasis N-glycan Tumorigenesis
SubtypeArticle
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
DOI10.1002/cbin.10707
Indexed BySCI
Language英语
WOS KeywordCancer Cells ; E-cadherin ; Acetylglucosaminyltransferase-iii ; Breast-cancer ; Growth ; Activation ; Metastasis ; Microenvironment ; Glycosylation ; Morphogenesis
WOS Research AreaCell Biology
WOS SubjectCell Biology
Funding OrganizationNational High Technology Research and Development Program of China (863 Program)(2014AA093604) ; Ocean Public Welfare Scientific Research Project, State Oceanic Administration of China(201405003)
WOS IDWOS:000393312200002
Citation statistics
Document Type期刊论文
Identifierhttp://ir.ipe.ac.cn/handle/122111/21925
Collection研究所(批量导入)
Affiliation1.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
Recommended Citation
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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