Suberoylanilide hydroxamic acid inhibits LX2 cells proliferation via decreasing yes-associated protein/transcriptional coactivator with PDZ-binding motif proteins

Background: Hepatic fibrosis is a complex and dynamic process similar to "wound healing" that results in the progressive accumulation of connective tissue. We aimed to investigate the epigenetic control of liver fibrosis and Hippo pathway in human hepatic stellate cell (HSC) line. We examined the effect of Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor on the LX2 cell line. Material and methods: 2.5 mu M SAHA was treated to LX2 cell line for 2 days. Cell proliferation and apoptosis measurement were performed by Muse Cell Analyzer. Yes-Associated Protein/Transcriptional Coactivator With Pdz-Binding Motif (YAP/TAZ) and alpha-smooth muscle actin (alpha-SMA) protein expression levels were measured by western blotting. Results: In our study, we observed that the SAHA treatment reduced cell viability and induced apoptosis of LX2 cells statistically. We found that SAHA treatment decreased alpha-SMA, YAP and TAZ proteins levels statistically. Conclusion: Decreased cell viability could be due to physiological, autophagical and also related to the apoptotical mechanisms. We thought that SAHA plays an important role in the creation of the fates of the LX2 cell line.