Please use this identifier to cite or link to this item:
Title: Potential Therapeutics Targeting Upstream Regulators and Interactors of EHMT1/2
Authors: Ang, Gareth Chin Khye
Gupta, Amogh
Surana, Uttam 
Yap, Shirlyn Xue Ling
Taneja, Reshma 
Issue Date: 9-Jun-2022
Publisher: MDPI AG
Citation: Ang, Gareth Chin Khye, Gupta, Amogh, Surana, Uttam, Yap, Shirlyn Xue Ling, Taneja, Reshma (2022-06-09). Potential Therapeutics Targeting Upstream Regulators and Interactors of EHMT1/2. Cancers 14 (12) : 2855-2855. ScholarBank@NUS Repository.
Abstract: Euchromatin histone lysine methyltransferases (EHMTs) are epigenetic regulators responsible for silencing gene transcription by catalyzing H3K9 dimethylation. Dysregulation of EHMT1/2 has been reported in multiple cancers and is associated with poor clinical outcomes. Although substantial insights have been gleaned into the downstream targets and pathways regulated by EHMT1/2, few studies have uncovered mechanisms responsible for their dysregulated expression. Moreover, EHMT1/2 interacting partners, which can influence their function and, therefore, the expression of target genes, have not been extensively explored. As none of the currently available EHMT inhibitors have made it past clinical trials, understanding upstream regulators and EHMT protein complexes may provide unique insights into novel therapeutic avenues in EHMT-overexpressing cancers. Here, we review our current understanding of the regulators and interacting partners of EHMTs. We also discuss available therapeutic drugs that target the upstream regulators and binding partners of EHMTs and could potentially modulate EHMT function in cancer progression.
Source Title: Cancers
ISSN: 20726694
DOI: 10.3390/cancers14122855
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
Ang et al revised .pdfAccepted version997.33 kBAdobe PDF



Google ScholarTM



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.