A correlation between altered O-GlcNAcylation, migration and with changes in E-cadherin levels in ovarian cancer cells

被引:42
作者
Jin, Feng-zhen [1 ,2 ]
Yu, Chao [2 ]
Zhao, De-zhang [2 ]
Wu, Ming-jun [2 ]
Yang, Zhu [1 ,2 ]
机构
[1] Chongqing Med Univ, Affiliated Hosp 2, Dept Obstet & Gynecol, Chongqing 400010, Peoples R China
[2] Chongqing Med Univ, Inst Life Sci, Chongqing 400016, Peoples R China
关键词
O-linked beta-N-acetylglucosamine transferase; O-GlcNAcylation; E-cadherin; Cell migration; Ovarian cancer; BETA-N-ACETYLGLUCOSAMINE; INSULIN-RESISTANCE; GLCNAC MODIFICATION; NUTRIENT SENSOR; C-MYC; GLYCOSYLATION; TRANSFERASE; PHOSPHORYLATION; ADHESION; CATENIN;
D O I
10.1016/j.yexcr.2013.03.013
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
O-GlcNAcylation is a dynamic and reversible posttranslational modification of nuclear and cytoplasmic proteins. In recent years, the roles of O-GlcNAcylation in several human malignant tumors have been investigated, and O-GlcNAcylation was found to be linked to cellular features relevant to metastasis. In this study, we modeled four diverse ovarian cancer cells and investigated the effects of O-GlcNAcylation on ovarian cancer cell migration. We found that total O-GlcNAcylation level was elevated in HO-8910PM cells compared to OVCAR3 cells. Additionally, through altering the total O-GlcNAcylation level by OGT silencing or OGA inhibition, we found that the migration of OVCAR3 cells was dramatically enhanced by PUGNAc and Thiamet G treatment, and the migration ability of HO-8910PM cells was significantly inhibited by OGT silencing. Furthermore, we also found that the expression of E-cadherin, an O-GlcNAcylated protein in ovarian cancer cells, was reduced by OGA inhibition in OVCAR3 cells and elevated by OGT silencing in HO-8910PM cells. These results indicate that O-GlcNAcylation could enhance ovarian cancer cell migration and decrease the expression of E-cadherin. Our studies also suggest that O-GlcNAcylation might become another potential target for the therapy of ovarian cancer. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:1482 / 1490
页数:9
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