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Review
. 2022 May 13;14(10):2402.
doi: 10.3390/cancers14102402.

Nuclear Receptor Coregulators in Hormone-Dependent Cancers

Hedieh Jafari  1   2 , Shahid Hussain  2 , Moray J Campbell  2
Affiliations
Review

Nuclear Receptor Coregulators in Hormone-Dependent Cancers

Hedieh Jafari et al. Cancers (Basel). .

Abstract

Nuclear receptors (NRs) function collectively as a transcriptional signaling network that mediates gene regulatory actions to either maintain cellular homeostasis in response to hormonal, dietary and other environmental factors, or act as orphan receptors with no known ligand. NR complexes are large and interact with multiple protein partners, collectively termed coregulators. Coregulators are essential for regulating NR activity and can dictate whether a target gene is activated or repressed by a variety of mechanisms including the regulation of chromatin accessibility. Altered expression of coregulators contributes to a variety of hormone-dependent cancers including breast and prostate cancers. Therefore, understanding the mechanisms by which coregulators interact with and modulate the activity of NRs provides opportunities to develop better prognostic and diagnostic approaches, as well as novel therapeutic targets. This review aims to gather and summarize recent studies, techniques and bioinformatics methods used to identify distorted NR coregulator interactions that contribute as cancer drivers in hormone-dependent cancers.

Keywords: breast cancer; chromatin; coactivators; corepressors; epigenetic; hormone dependent cancers; nuclear receptors; prostate cancer; therapy resistance; transcriptome.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic model of NR-target gene transcriptional activation (left panel) and repression (right panel).
See this image and copyright information in PMC

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