Histone deacetylase 7 silencing induces apoptosis and autophagy in salivary mucoepidermoid carcinoma cells

Background The overexpression of histone deacetylases ( HDAC s) has been observed in many cancers, and inhibition of specific HDAC s has emerged as a new target for cancer therapy. We found that HDAC 7 expression was selectively reduced by HDAC inhibitor apicidin in salivary mucoepidermoid carcinoma ( MEC ) cells. Here, we show that HDAC 7 suppression has a potent antitumor effect in MEC cells. Methods Histone deacetylases7 was knocked down using HDAC 7 si RNA s, and cell proliferation was quantified. Cell cycle progression, apoptosis, and autophagy were measured by flow cytometry and immunoblotting. Results Histone deacetylases 7 si RNA s inhibited cell proliferation and c‐Myc expression, increased p27 expression, and caused G2/M phase cell cycle arrest in both YD ‐15 and Mc3 cells. HDAC 7 silencing increased the sub‐G1 population, Annexin V positive apoptotic cells and cleaved caspase3 levels. HDAC 7 silencing induced an increase in autophagic markers, number of acidic vesicular organelles, and LC 3B II levels, and decrease in p62 levels. HDAC 7 si RNA s reduced the activation of ERK . HDAC 7 knockdown resulted in growth inhibition through G2/M phase cell cycle arrest and induced both apoptosis and autophagy in MEC cells. Conclusions This study indicates that inhibition of HDAC 7 might become a novel and effective therapeutic approach for treating to MEC .