Altered beta 1,6-GlcNAc branched N-glycans impair TGF-beta-mediated Epithelial-to-Mesenchymal Transition through Smad signalling pathway in human lung cancer
文献类型:期刊论文
作者 | Li, N; Xu, HN; Fan, K; Liu, XJ; Qi, JJ; Zhao, C; Yin, P; Wang, LY; Li, ZX; Zha, XL |
刊名 | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
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出版日期 | 2014 |
卷号 | 18期号:10页码:1975-1991 |
关键词 | GnT-V N-glycans lung cancer EMT TGF-1 |
通讯作者 | Li, ZX (reprint author), Fudan Univ, Dept Biochem & Mol Biol, Shanghai Med Coll, 138 Yi Xue Yuan Rd, Shanghai 200032, Peoples R China.,lizengxia@fudan.edu.cn ; xlzha@shmu.edu.cn |
英文摘要 | The change of oligosaccharide structure has been revealed to be crucial for glycoproteins' biological functions and cell biological characteristics. N-acetylglucosaminy transferase V (GnT-V), a key enzyme catalysing the reaction of adding 1, 6-N-acetylglucosamine (GlcNAc) on asparagine-linked oligosaccharides of cell proteins, has been implicated to a metastastic-promoting oncoprotein in some carcinomas. However, this correlation might not be subjected to all types of cancers, for example, in non-small cell lung cancers, low level of GnT-V expression is associated with relatively short survival time and poor prognosis. To explain the role of GnT-V in lung cancer progression, we studied the association of GnT-V expression with lung cancer EMT behaviour. We found that GnT-V expression was correlated with epithelial marker positively and mesenchymal marker negatively. GnT-V levels, as well as 1,6-GlcNAc branched N-glycans, were strongly reduced in TGF-1-induced EMT of human lung adenocarcinoma A549 cells. Further studies showed that suppression of 1,6-GlcNAc branched N-glycans by inhibitor or GnT-V silencing in A549 cells could promote TGF-1-induced EMT-like changes, cell migration and invasion. Meanwhile, overexpression of GnT-V impaired TGF-1-induced EMT, migration and invasion. It suggests that GnT-V suppresses the EMT process of lung cancer cells through inhibiting the TGF-/Smad signalling and its downstream transcription factors in a GnT-V catalytic activity-dependent manner. Taken together, the present study reveals a novel mechanism of GnT-V as a suppressor of both EMT and invasion in human lung cancer cells, which may be useful for fully understanding N-glycan's biological roles in lung cancer progression. |
学科主题 | Cell Biology; Research & Experimental Medicine |
类目[WOS] | Cell Biology ; Medicine, Research & Experimental |
关键词[WOS] | FOCAL ADHESION KINASE ; ACETYLGLUCOSAMINYLTRANSFERASE-V ; TUMOR PROGRESSION ; CELL-LINES ; LINKED OLIGOSACCHARIDES ; BREAST-CARCINOMA ; GENE-EXPRESSION ; MESSENGER-RNA ; GROWTH ; GLYCOSYLATION |
收录类别 | SCI |
语种 | 英语 |
WOS记录号 | WOS:000343739200007 |
版本 | 出版稿 |
源URL | [http://202.127.25.143/handle/331003/235] ![]() |
专题 | 上海生化细胞研究所_上海生科院生化细胞研究所 |
推荐引用方式 GB/T 7714 | Li, N,Xu, HN,Fan, K,et al. Altered beta 1,6-GlcNAc branched N-glycans impair TGF-beta-mediated Epithelial-to-Mesenchymal Transition through Smad signalling pathway in human lung cancer[J]. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,2014,18(10):1975-1991. |
APA | Li, N.,Xu, HN.,Fan, K.,Liu, XJ.,Qi, JJ.,...&Zha, XL.(2014).Altered beta 1,6-GlcNAc branched N-glycans impair TGF-beta-mediated Epithelial-to-Mesenchymal Transition through Smad signalling pathway in human lung cancer.JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,18(10),1975-1991. |
MLA | Li, N,et al."Altered beta 1,6-GlcNAc branched N-glycans impair TGF-beta-mediated Epithelial-to-Mesenchymal Transition through Smad signalling pathway in human lung cancer".JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 18.10(2014):1975-1991. |
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