INTRODUCTION: Liver fibrosis stimulates the abnormal wound repair response of chronic tissue damage, leading to the emergence of many chronic liver diseases such as cirrhosis. In addition, this process is characterized by excessive accumulation of extracellular matrix (ECM) components. The activation of silent hepatic stellate cells (HSCs) in liver fibrosis leads to the release of more ECM. HOX transcript antisense RNA (HOTAIR) is a long non-coding RNAs (lncRNAs) that are overexpressed in numerous types of cancer and are also associated with a number of various fibrosis processes. Recent studies have shown that lncRNAs are important in epigenetic modification. In our study, we aimed to evaluate the effect of the epigenetic drugs suberoylanilide hydroxamic acid (SAHA) and 3-deazaneplanocin A (DZNep) on HOTAIR expression in HSC line (LX2).
METHODS: LX2 cells were scraped with TRIzol using a scraper and total RNAs were taken into ependorphs. After cDNA synthesis from RNA was obtained with the appropriate kit, cDNAs were amplified with FAM-labeled primer probes specific to the mRNA sequence of the genes HOTAIR expression levels which were calculated 2(-ΔΔ)(CT) method and GAPDH was used for control gene.
RESULTS: Both SAHA and DZNep statistically decreased HOTAIR gene levels in LX2 cells (p<0.001; p<0.001, respectively).
DISCUSSION AND CONCLUSION: Due to the fact that both DZNep and SAHA reduced HOTAIR expression, it can be thought that the combined use of both drugs synergistically could be an important approach in preventing hepatic fibrosis. However, further mechanisms related to HOTAIR inhibition should be investigated in hepatic fibrosis.