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

ECM1通过诱导上皮间质转化促进肝细胞癌的迁移和侵袭

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作者:Hao Chen, Weidong Jia, Jiansheng Li

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.

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.

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.

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