KAI1 reverses the epithelial-mesenchymal transition in human pancreatic cancer cells

被引:5
作者
Liu, Xu [1 ]
Guo, Xiao-Zhong [1 ]
Li, Hong-Yu [1 ]
Chen, Jiang [1 ]
机构
[1] Gen Hosp, Shenyang Mil Area, Dept Gastroenterol, 83 Wenhua Rd, Shenyang 110840, Liaoning, Peoples R China
基金
中国国家自然科学基金;
关键词
KAI1; Epithelial-mesenchymal transition; Pancreatic cancer; EXPRESSION; METASTASIS; ACTIVATION; VIMENTIN; ADHESION; SNAIL;
D O I
10.1016/j.hbpd.2019.03.004
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: Epithelial-mesenchymal transition (EMT) plays an important role in pancreatic cancer (PC). In the present study, we investigated the effects of KAI1 gene overexpression on the EMT of human PC cell lines, MIA PaCa-2 and PACN-1. Methods: Plasmids overexpressing KAI1 and pCMV were transfected into MIA PaCa-2 and PACN-1 cells, respectively. After selection of differently transfected cells by G418, KAI1 protein levels were examined by Western blotting, and transfected cells were renamed as MIA PaCa-2-K, MIA PaCa-2-p, PACN-1-K and PACN-1-p. Wound healing and Transwell migration assays were then performed comparing the two groups of cells. EMT-related markers were analyzed by Western blotting. Results: The percentage of wound closure significantly decreased in MIA PaCa-2-K cells compared with MIA PaCa-2-p and MIA PaCa-2 cells after 24, 48 and 72 h (P < 0.05). In PACN-1-K cells, the percentage of wound closure significantly decreased as well (P < 0.05). Numbers of invading MIA PaCa-2, MIA PaCa-2-p and MIA PaCa-2-K cells were determined as 48.0 +/- 15.4, 50.0 +/- 12.4, and 12.0 +/- 3.8, respectively. The corresponding numbers of invading PACN-1, PACN-1-p and PACN-1-K cells were 29.0 +/- 10.6, 31.0 +/- 11.4, and 8.0 +/- 4.2, respectively. KAI1 overexpression induced a significant upregulation of E-cadherin and also significant downregulation of Snail, vimentin, matrix metalloproteinase 2 (MMP2) and MMP9 (all P < 0.05) in PC cells. Conclusions: KAI1 reversed EMT-related marker expression and inhibited migration and invasion of PC cells. Thus, KAI1 might represent a novel potential therapeutic target for PC. (C) 2019 First Affiliated Hospital, Zhejiang University School of Medicine in China. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:471 / 477
页数:7
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