Minireview: Nuclear Receptor Coregulators of the p160 Family: Insights into Inflammation and Metabolism

Rollins, David A.; Coppo, Maddalena; Rogatsky, Inez

doi:10.1210/me.2015-1005

Cited by 53 publications

(34 citation statements)

References 132 publications

(152 reference statements)

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“…The VN1R1 gene, on the other hand, has not been previously related to human cancer. Nuclear recep-tor coactivator 2 (NCOA2) is a transcription factor that plays important roles in cell growth, development, and homeostasis (Stashi et al, 2014;Rollins et al, 2015). It has been previously associated with human malignant tumors, including PCa (Taylor et al, 2010) where it acts as an androgen receptor coactivator (Agoulnik et al, 2005), being therefore linked to PCa progression.…”

Section: Discussionmentioning

confidence: 99%

NCOA2 is a candidate target gene of 8q gain associated with clinically aggressive prostate cancer

Silva

Barros-Silva

Vieira

et al. 2016

Genes Chromosomes & Cancer

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Prostate carcinomas harboring 8q gains are associated with poor clinical outcome, but the target genes of this genomic alteration remain to be unveiled. In this study, we aimed to identify potential 8q target genes associated with clinically aggressive prostate cancer (PCa) using fluorescence in situ hybridization (FISH), genome-wide mRNA expression, and protein expression analyses. Using FISH, we first characterized the relative copy number of 8q (assessed with MYC flanking probes) of a series of 50 radical prostatectomy specimens, with available global gene expression data and typed for E26 transformation specific (ETS) rearrangements, and then compared the gene expression profile of PCa subsets with and without 8q24 gain using Significance Analysis of Microarrays. In the subset of tumors with ERG fusion genes (ERG+), five genes were identified as significantly overexpressed (false discovery rate [FDR], ≤ 5%) in tumors with relative 8q24 gain, namely VN1R1, ZNF417, CDON, IKZF2, and NCOA2. Of these, only NCOA2 is located in 8q (8q13.3), showing a statistically higher mRNA expression in the subgroup with relative 8q gain, both in the ERG+ subgroup and in the whole series (P = 0.000152 and P = 0.008, respectively). Combining all the cases with NCOA2 overexpression, either at the mRNA or at the protein level, we identified a group of tumors with NCOA2 copy-number increase, independently of ETS status and relative 8q24 gain. Furthermore, for the first time, we detected a structural rearrangement involving NCOA2 in PCa. These findings warrant further studies with larger series to evaluate if NCOA2 relative copy-number gain presents prognostic value independently of the well-established poor prognosis associated with MYC relative copy-number gain.

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Section: Discussionmentioning

confidence: 99%

NCOA2 is a candidate target gene of 8q gain associated with clinically aggressive prostate cancer

Silva

Barros-Silva

Vieira

et al. 2016

Genes Chromosomes & Cancer

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“…Both whole-body and liver-specific ablation of Src2 phenocopies a Von Gierke–like disease that is characterized by fasting hypoglycaemia, hepatic steatosis and increased circulating levels of triglycerides, cholesterol and FFAs 74 . Hepatic SRC3 mRNA and protein levels increase upon HFD feeding, and genetic ablation of Src3 protects against HFD-induced hepatic steatosis by reducing lipid accumulation and the accompanying inflammatory response 75,76,77 . Whole-body genetic ablation of Pgc1a/b (encoding PGC1α/β) results in increased hepatic steatosis, although liver-specific deletion is needed to confirm whether these effects are intrinsic to the liver 78–80 .…”

Section: Liver Fat Metabolism and Edcsmentioning

confidence: 99%

Endocrine-disrupting chemicals and fatty liver disease

et al. 2017

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Nonalcoholic fatty liver disease (NAFLD) is a growing epidemic paralleling the increase in obesity and diabetes mellitus seen in Western diet-consuming countries. As NAFLD can lead to life-threatening conditions such as cirrhosis and hepatocellular carcinoma (HCC), an understanding of factors that trigger its development and pathological progression is needed. Although by definition this disease is not associated with alcohol consumption, exposure to environmental agents that have been linked to other diseases might have a role in the development of NAFLD. Here, we focus on one class of these agents, endocrine-disrupting chemicals (EDCs), and their potential to influence the initiation and progression of a cascade of pathological conditions associated with fatty liver. Experimental studies have revealed several potential mechanisms by which EDC exposures might contribute to disease pathogenesis, including modulation of nuclear hormone receptor (NR) function and alteration of the epigenome. However, many questions remain to be addressed about the causal link between acute and chronic EDC exposure and the development of NAFLD in humans. Future studies that address these questions hold promise not only for understanding the linkage between EDC exposure and liver disease, but for elucidating the molecular mechanisms underpinning NAFLD and the development of new prevention and treatment opportunities.

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“…The importance for these proteins in diverse biological processes including metabolism, circadian rhythm, immunity and reproduction as revealed by gene ablation studies in mice has been extensively reviewed elsewhere [49–51]. …”

Section: Gr and Its Coregulatorsmentioning

confidence: 99%

There goes the neighborhood: Assembly of transcriptional complexes during the regulation of metabolism and inflammation by the glucocorticoid receptor

et al. 2016

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Glucocorticoids (GCs), as ligands for the glucocorticoid receptor (GR), represent one of the most effective and frequently used classes of drugs for anti-inflammatory and immunosuppressive therapy. In addition, its role in physiological and pathophysiological processes makes the GR an important research target. The past decades have yielded a wealth of insight into the physiological and pharmacological effects of GCs. Today’s era of next generation sequencing techniques is now beginning to elucidate the molecular and genomic circuits underlying GR’s cell type-specific actions. This review focuses on the concepts and insights gained from recent studies in two of the most important tissues for GC action: the liver (mediating GR’s metabolic effects) and macrophages (as the main target of anti-inflammatory GC therapy). We summarize results obtained from transgenic mouse models, molecular and genome-wide studies to illustrate GR’s complex interactions with DNA, chromatin, co-regulators and other transcription factors. Characterizing the cell type-specific transcriptional complexes assembled around GR will pave the road for the development of new anti-inflammatory and metabolic therapies in the future.

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Minireview: Nuclear Receptor Coregulators of the p160 Family: Insights into Inflammation and Metabolism

Cited by 53 publications

References 132 publications

NCOA2 is a candidate target gene of 8q gain associated with clinically aggressive prostate cancer

NCOA2 is a candidate target gene of 8q gain associated with clinically aggressive prostate cancer

Endocrine-disrupting chemicals and fatty liver disease

There goes the neighborhood: Assembly of transcriptional complexes during the regulation of metabolism and inflammation by the glucocorticoid receptor

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