Figure 3.

Epigenomic dysregulation in uterine leiomyoma and potential therapeutic targets. Histone modification (1), aberrant promoter methylation (2) and altered enhancer architecture (3) are three categories of epigenomic changes that are implicated in the pathogenesis of uterine leiomyomas. Epi-drugs (HDACi indicates histone deacetylase inhibitor; HATi, histone acetyltransferase inhibitor; BETi, bromodomain and extra-terminal motif protein inhibitor; HDMi, histone demethylase inhibitor; HMTi, histone methyltransferase inhibitor; TETi, ten-eleven translocation protein inhibitor; DNMTi, DNA methyltransferase inhibitor), which target the enzymes involved in modulating epigenomic marks (HDAC indicates histone deacetylase; HAT, histone acetyltransferase; BRD, bromodomain protein; HDM, histone demethylase; HMT, histone methyltransferase; TET, ten-eleven translocation protein; DNMT, DNA methyltransferase), may play a critical role in managing tumor development. Adapted from ‘Regulation of Transcription in Eukaryotic Cells’, by BioRender.com (2020). Retrieved from https://app.biorender.com/biorender-templates