IGFBP2 promotes the EMT of colorectal cancer cells by regulating E-cadherin expression

被引:4
作者
Zhu, Huange [1 ]
Zhang, Yanping [1 ]
Geng, Yan [1 ]
Lu, Wei [1 ]
Yin, Jian [1 ]
Li, Zhenzhen [1 ]
Huang, Lun [1 ]
Liu, Hailong [1 ]
Xu, Nan [1 ]
机构
[1] Xi An Jiao Tong Univ, Xibei Hosp, Affiliated Hosp 2, Clin Lab, 157 Xiwu Rd, Xian 710004, Shaanxi, Peoples R China
来源
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY | 2019年 / 12卷 / 07期
关键词
Colorectal cancer; insulin like growth factor binding protein 2 (IGFBP2); epithelial-mesenchymal transition (EMT); E-cadherin; FACTOR-BINDING PROTEIN-2; GROWTH; GLIOBLASTOMA; PROLIFERATION; BIOMARKER; INVASION; PATHWAY; COLON; RISK;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
This study aimed to investigate the expression of insulin like growth factor binding protein 2 (IGFBP2) in colorectal cancer cells and its effect on the biological characteristics of cancer cells. We first established IGFBP2 knockdown (HCT116-shIGFBP2) and overexpression (HT29-IGFBP2) cell lines. Western blotting was used to evaluate the overexpression and knockdown efficiency. Next, the effect of IGFBP2 on colorectal cancer cell proliferation and migration was evaluated through cell proliferation and wound healing assays, respectively. Cell proliferation experiments showed that the upregulation of IGFBP2 promoted the proliferation of HT29 cells, but the downregulation of IGFBP2 inhibited the proliferation of HCT116 cells. Moreover, a wound healing assay showed that the migration ability of HCT116 cells was significantly reduced after the downregulation of IGFBP2. Also, the level of E-cadherin in HCT116-shIGFBP2 cells was significantly upregulated following IGFBP2 knockdown. Further analyses showed that colorectal cancer cells secreted high levels of IGFBP2 into the extracellular matrix, which inhibited E-cadherin expression as well. Overall, the results of this study showed that IGFBP2 inhibits the expression of E-cadherin and promotes the proliferation and migration of colorectal cancer cells.
引用
收藏
页码:2559 / 2565
页数:7
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