CAS OpenIR  > 研究所(批量导入)
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
发表期刊CELL BIOLOGY INTERNATIONAL
ISSN1065-6995
卷号41期号:2页码:124-133
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.
关键词Bisecting Glcnac Epidermal Growth Factor Epithelial-mesenchymal Transition Metastasis N-glycan Tumorigenesis
文章类型Article
WOS标题词Science & Technology ; Life Sciences & Biomedicine
DOI10.1002/cbin.10707
收录类别SCI
语种英语
关键词[WOS]CANCER CELLS ; E-CADHERIN ; ACETYLGLUCOSAMINYLTRANSFERASE-III ; BREAST-CANCER ; GROWTH ; ACTIVATION ; METASTASIS ; MICROENVIRONMENT ; GLYCOSYLATION ; MORPHOGENESIS
WOS研究方向Cell Biology
WOS类目Cell Biology
项目资助者National High Technology Research and Development Program of China (863 Program)(2014AA093604) ; Ocean Public Welfare Scientific Research Project, State Oceanic Administration of China(201405003)
WOS记录号WOS:000393312200002
引用统计
文献类型期刊论文
条目标识符http://ir.ipe.ac.cn/handle/122111/21925
专题研究所(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.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Xu, Qingsong]的文章
[Qu, Chen]的文章
[Wang, Wenjing]的文章
百度学术
百度学术中相似的文章
[Xu, Qingsong]的文章
[Qu, Chen]的文章
[Wang, Wenjing]的文章
必应学术
必应学术中相似的文章
[Xu, Qingsong]的文章
[Qu, Chen]的文章
[Wang, Wenjing]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。