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ECM1 promotes migration and invasion of hepatocellular carcinoma by inducing epithelial-mesenchymal transition

Authors :
Jian-Sheng Li
Wei-Dong Jia
Hao Chen
Source :
World Journal of Surgical Oncology
Publication Year :
2016
Publisher :
Springer Science and Business Media LLC, 2016.

Abstract

Background Extracellular matrix protein 1 (ECM1) is a glycoprotein involved in many biologic processes. To determine the expression of ECM1 in hepatocellular carcinoma (HCC), and to study the role of ECM1 in inducing epithelia-mesenchymal transition (EMT) to analyze the effect of ECM1 on the migration and invasion of HCC cells. Methods The expression of ECM1 in HCC specimens was examined by immunohistochemistry staining, and the correlations were analyzed between the expression of ECM1 and the clinicopathological data. The ECM1 expression plasmid was transfected into Bel-7402 cells to induce exogenous overexpression of ECM1 protein. The changes of the expression of ECM1, EMT-related protein (E-cadherin, Vimentin), in Bel-7402 cells were detected by Western blot after transfection of ECM1; the wound healing and invasion assay in vitro were used to determine the role of ECM1 gene transfection on the ability of migration and invasive potential of Bel-7402 cells. Results Immumohistochemistry staining method displayed the ECM1 expression was positively associated with vascular invasion, TNM stage, and poor prognosis. A significant positive correlation was found between the expressions of ECM1 and Vimentin. After ECM1 overexpression, Western blot exhibited that the expression of E-cadherin was down-regulated and Vimentin expression was up-regulated in Bel-7402 cells; the wound healing and invasion assay showed that the migration and invasion potentials of Bel-7402 cells were significantly enhanced. Conclusions ECM1, which displayed a high expression in HCC specimens, was closely associated with clinicopathologic data and may promote migration and invasion of HCC cells by inducing EMT. Electronic supplementary material The online version of this article (doi:10.1186/s12957-016-0952-z) contains supplementary material, which is available to authorized users.

Details

ISSN :
14777819
Volume :
14
Database :
OpenAIRE
Journal :
World Journal of Surgical Oncology
Accession number :
edsair.doi.dedup.....299f8cf9b92187cea1584b516fd20d36
Full Text :
https://doi.org/10.1186/s12957-016-0952-z