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Histone deacetylase 7 silencing induces apoptosis and autophagy in salivary mucoepidermoid carcinoma cells
Author(s) -
Ahn MeeYoung,
Yoon JungHoon
Publication year - 2017
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12560
Subject(s) - mucoepidermoid carcinoma , autophagy , apoptosis , histone deacetylase , cancer research , gene silencing , histone , salivary gland , medicine , chemistry , biology , pathology , genetics , gene
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 .