Matrix Metalloproteinase (MMP)-12 Promote Invasion and Migration of Esophageal Squamous Cell Carcinoma Cell by Epithelial-Mesenchymal Transition

被引:0
作者
Shi, Dong-Hui [1 ]
Jin, Jiang [2 ]
机构
[1] Yancheng First Peoples Hosp, Dept Thorac & Cardiovasc Surg, Yancheng 224006, Peoples R China
[2] Wenzhou Med Univ, Taizhou Hosp Zhejiang Prov, Dept Cardiothorac Surg, Linhai 317000, Peoples R China
关键词
Esophageal Squamous Cell Carcinoma; Matrix Metalloproteinase-12; Epithelial-Mesenchymal Transition; Invasion; Migration; E-CADHERIN; ADHESION COMPLEX; CANCER INVASION; LUNG-CANCER; EXPRESSION; MMP-12; OVEREXPRESSION; METASTASIS; TUMOR;
D O I
10.1166/jbt.2019.2100
中图分类号
Q813 [细胞工程];
学科分类号
摘要
The present study aimed to investigate the role of matrix metalloproteinase (MMP)-12 on cell migration and invasion of esophageal squamous cell carcinoma (ESCC) though epithelial-mesenchymal transition (EMT). The ESCC cell lines (ECA-109, KYSE-30, KYSE-410, KYSE-520) and normal esophageal epithelial cells (HEEC) were cultured. ECA-109 cells were then chosen to be transfected with the plasmids of MMP-12 over-expression, MMP-12 inhibitor, E-cad over-expression and empty control vectors. The protein and mRNA levels of MMP-12 were detected using western blot and qRT-PCR analysis. Transwell and wound healing assays were used to assess cell invasion and migration. Results indicated that MMP-12 was upregulated significantly in all the ESCC cell lines. Overexpression of MMP-12 increased MMP-12 expression, and the abilities of invasion and migration of ECA-109 cells. Overexpression of MMP-12 increased the expression of N-cad and vimentin, but decreased E-cad expression. Additionally, we found that cells treated with inhibitor-MMP-12 were opposite to the above results. Moreover, up-regulation of E-cad were eliminated all effects on ECA-109 cells caused by MMP-12 over-expression. In conclusion, MMP-12 promoted ECA-109 cells migration and invasion by the alteration of the EMT marker protein, which is one of its mechanisms. Therefore, MMP-12 may be a new therapeutic target for ESCC.
引用
收藏
页码:1120 / 1126
页数:7
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