The regulatory mechanism of histone deacetylases in epigenetic regulation: emerging paradigms from hdac inhibition studies in uterine leiomyosarcoma

Uterine leiomyosarcoma (LMS) is an aggressive and the most common type of uterine sarcoma that presents a poor prognosis, high rates of recurrence, and metastasis. Currently, there is limited information available concerning molecular mechanisms of LMS development and pathogenesis. Class I histone deacetylases (including HDAC1, 2, 3, and 8) are one of the major classes of the HDAC family, catalyzing the removal of acetyl groups from lysine residues in histones and cellular proteins. In this study, we aim to assess the transcriptome of LMS in the presence or absence of class I histone deacetylases (HDAC) inhibitor (HDACi, tucidinostatin), and characterized the regulatory mechanism of class I HDACs in the pathogenesis of LMS.