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Histone deacetylase (HDAC) inhibitors are emerging as a novel class of anti-tumor agents and have manifested the ability to decrease proliferation and increase apoptosis in different cancer cells. A significant number of genes have been identified as potential effectors responsible for the anti-tumor function of HDAC inhibitor. However, the molecular mechanisms of these HDAC inhibitors in this process remain largely undefined. In the current study, we searched for microRNAs (miRs) that were affected by HDAC inhibitor trichostatin (TSA) and investigated their effects in endometrial cancer (EMC) cells. Our data showed that TSA significantly inhibited the growth of EMC cells and induced their apoptosis. Among the miRNAs that altered in the presence of TSA, the  miR-106b-93-25  cluster, together with its host gene  MCM7 , were obviously down-regulated in EMC cells.  p21  and  BIM , which were identified as target genes of  miR-106b-93-25  cluster, increased in TSA treated tumor cells and were responsible for cell cycle arrest and apoptosis. We further identified  MYC  as a regulator of  miR-106b-93-25  cluster and demonstrated its down-regulation in the presence of TSA resulted in the reduction of  miR-106b-93-25  cluster and up-regulation of  p21  and  BIM . More important, we found  miR-106b-93-25  cluster was up-regulated in clinical EMC samples in association with the overexpression of  MCM7  and  MYC  and the down-regulation of  p21  and  BIM . Thus our studies strongly indicated TSA inhibited EMC cell growth and induced cell apoptosis and cell cycle arrest at least partially through the down-regulation of the  miR-106b-93-25  cluster and up-regulation of it's target genes  p21  and  BIM  via  MYC .

TSA Suppresses miR-106b-93-25 Cluster Expression through Downregulation of MYC and Inhibits Proliferation and Induces Apoptosis in Human EMC