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The histone deacetylase inhibitor trichostatin A alters microRNA expression profiles in apoptosis-resistant breast cancer cells.

The development of drug resistance represents a major complication in the             effective treatment of breast cancer. Epigenetic therapy, through the use of histone             deacetylase inhibitors (HDACi) or demethylation agents, is an emerging area of             therapeutic targeting in a number of ontological entities, particularly in the             setting of aggressive therapy-resistant disease. Using the well-described HDAC             inhibitor trichostatin A (TSA) we demonstrate the suppression of in vitro clonogenicity             in the previously described apoptosis-resistant MCF-7TN-R breast carcinoma cell             line. Additionally, recent work has demonstrated that these agents can alter the             expression profile of microRNA signatures in malignant cells. Using an unbiased             microRNA microarray analysis, changes in miRNA expression of MCF-7TN-R cells treated             with TSA for 24 h were analyzed. We observed significant up-regulation of 22 miRNAs             and down-regulation of 10 miRNAs in response to TSA treatment. Our results demonstrate             that the HDACi, TSA, exerts anticancer activity in the apoptosis-resistant MCF-7TN-R             breast carcinoma cell line. This activity is correlated with TSA alteration of             microRNA expression profiles indicative of a less aggressive phenotype.