Downregulation of matrix metalloproteinases contributes to the inhibition of cell migration and invasion in HepG2 cells by sodium valproate.

Abstract

Histone deacetylation levels are closely associated with the genesis and development of tumors. However, the anti-tumor effect and mechanism of class I histone deacetylase inhibitor sodium valproate (VPA) on hepatocellular carcinoma cells has not been demonstrated clearly. In the present study, HepG2 hepatocellular carcinoma cells were exposed to VPA, and the effects of VPA on the proliferation, apoptosis, metastasis and invasion of the cells were evaluated. The MTT method and colony assays were used to detect cell proliferation, and cell migration and Transwell invasion were also evaluated. In addition, the protein expression levels of matrix metalloproteinase (MMP)-2 and MMP-9 were measured by flow cytometric analysis. The results indicated that VPA was able to inhibit proliferation and reverse the malignant phenotypes of hepatocellular carcinoma cells by inducing cell apoptosis. Furthermore, the colony formation and migration abilities of HepG2 cells were downregulated by VPA. Protein expression levels of MMP-2 and MMP-9 in HepG2 cells were also downregulated following VPA treatment, which contributed to suppression of the migration and invasion ability of HepG2 cells.