Abstract
Carcinogenesis is a complex process tightly regulated at multiple levels by post-translational modifications. Epigenetics plays a major role in cancer development, all stable changes to the gene expression process that are not a result of a direct change in the DNA code are described as epigenetics. Epigenetic processes are regulated by post-translational modifications including ubiquitination which can directly affect either histones or transcription factors or may target their co-factors and interacting partners exerting an indirect effect. Deubiquitination of these target proteins is equally important and alterations in this pathway can also lead to cancer development, progression and metastasis. Only the correct, unaltered balance between ubiquitination and deubiquitination ensures healthy cellular homeostasis. In this review we focus on the role of deubiquitinating (DUB) enzymes in various aspects of epigenetics including the regulation of transcription factors, histone modifications, DNA damage repair pathways and cell cycle regulation. We discuss the impact of those processes on tumourigenesis and potential therapeutic applications of DUBs for cancer treatment.
Highlights
Ubiquitination is one of the most important post-translation modifications (PTMs) responsible for regulating the stability and activity of modified proteins
Deubiquitination of histones, transcription factors and their co-factors plays a major role in regulating epigenetics by Deubiquitinating enzymes (DUBs)
As a result DUBs could be valuable therapeutic targets in oncology. This field is still relatively novel, recent advances indicate that targeting DUBs could be an efficient strategy
Summary
Ubiquitination is one of the most important post-translation modifications (PTMs) responsible for regulating the stability and activity of modified proteins. Usp12 was reported to deubiquitinate the AR resulting in its increased protein stability and transcriptional activity [12]. Usp42 forms a direct complex with p53 and controls its activation in response to cellular stress; as a result it regulates p53-dependent transcription and cell cycle arrest.
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