Effect of Valproic Acid on the Class I Histone Deacetylase 1, 2 and 3, Tumor Suppressor Genes p21WAF1/CIP1 and p53, and Intrinsic Mitochondrial Apoptotic Pathway, Pro- (Bax, Bak, and Bim) and anti- (Bcl-2, Bcl-xL, and Mcl-1) Apoptotic Genes Expression, Cell Viability, and Apoptosis Induction in Hepatocellular Carcinoma HepG2 Cell Line

Backgrounds: Hepatocellular carcinoma (HCC), Primary liver cancer, is the fifth most common cancer in men. Histone deacetylation causes chromatin condensation resulting gene silencing and tumorigenesis. These enzymes have become a novel target for treatment of cancer. deacetylase inhibitors (HDACIs) can reactivate tumor suppressor genes (TSGs) by inhibition histone deacetylases (HDACs) activity leads to apoptosis induction cells. Further, these compounds induce through intrinsic/mitochondrial pathway. Previously, we reported effect valproic acid (VPA) trichostatin A (TSA) on TSGs p21WAF1/CIP1 (p21), p27Kip1 (p27), p57Kip2 (P57) also HDAC1 colon The present study was designed investigate VPA class I (HDAC) 1, 2 3, p21and p53, intrinsic mitochondrial pathway, pro- (Bax, Bak, Bim) anti- (Bcl-2, Bcl-xL, Mcl-1) apoptotic genes, viability, HCC HepG2 cell line. Materials Methods: cells were cultured treated with VPA. To determine apoptosis, relative expression level mentioned MTT assay, qRT-PCR done respectively. Results: downregulated 2, Bcl-2, Mcl-1 upregulated p21, Bax, Bim induction. Conclusion: via activation pathway epigenetic reactivation p21 p53 HDAC activity.