The Effect of Quisinostat as the HDAC Inhibitor on Migration

Cancer cannot be explained only by genetic alterations but involves epigenetic processes. Modifying histones by acetylation plays a key role in epigenetic regulation of gene expression and is controlled by the balance between Histone Deacetylases (HDAC) and Histone Acetyltransferases (HAT). The HDACs expression and activity could be involved in several tumorigenesis mechanisms, so their inhibition induces cancer cell cycle arrest and migration.

Quisinostat is a novel promising second-generation HDAC inhibitor class of hydroxamic acid with high cellular potency towards classes I and II HDACs. Therefore, its low IC50 (<0.5nM) and bioavailability have been chosen to carry out our studies. Cancer cells were treated with Quiznos at nM200, and cell migration was measured by fluorescent microscopy.

This study was the result of a preliminary study of Shiraz University (Code: 96GCU3M1293).

 The data showed that treatment of cancer cells with Quiznos significantly (P<0.05) reduced cell migration. DMSO did not affect reducing cell migration.

 In this project try to explore the possible therapeutic application of this HDAC inhibitor against colon cancer. This study showed Quisinostat exerts broad-spectrum antiproliferative activity and migration.