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.
Purine-rich element binding protein alpha promotes invasion and migration of esophageal squamous cell carcinoma KYSE 510 cells by inducing epithelial-mesenchymal transition
