The nuclear receptor transcriptional coregulator RIP140

Augereau, Patrick; Badia, Eric; Carascossa, Sophie; Castet, Audrey; Fritsch, Samuel; Harmand, Pierre-Olivier; Jalaguier, Stéphan; Cavaillès, Vincent

doi:10.1621/nrs.04024

Cited by 51 publications

(53 citation statements)

References 75 publications

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“…RIP140 was also shown to interact with many other nuclear receptors (NRs) and transcription factors (for a review see ref. 7). More recently, we demonstrated that RIP140 behaves as an Rb-like regulator of the E2F pathway by directly binding to E2Fs and repressing their transactivation potentials (8).…”

Section: Introductionmentioning

confidence: 99%

RIP140 increases APC expression and controls intestinal homeostasis and tumorigenesis

Lapierre¹,

Bonnet²,

Bascoul-Mollevi³

et al. 2014

J. Clin. Invest.

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Deregulation of the Wnt/APC/β-catenin signaling pathway is an important consequence of tumor suppressor APC dysfunction. Genetic and molecular data have established that disruption of this pathway contributes to the development of colorectal cancer. Here, we demonstrate that the transcriptional coregulator RIP140 regulates intestinal homeostasis and tumorigenesis. Using Rip140-null mice and mice overexpressing human RIP140, we found that RIP140 inhibited intestinal epithelial cell proliferation and apoptosis. Interestingly, following whole-body irradiation, mice lacking RIP140 exhibited improved regenerative capacity in the intestine, while mice overexpressing RIP140 displayed reduced recovery. Enhanced RIP140 expression strongly repressed human colon cancer cell proliferation in vitro and after grafting onto nude mice. Moreover, in murine tissues and human cancer cells, RIP140 stimulated APC transcription and inhibited β-catenin activation and target gene expression. Finally, RIP140 mRNA and RIP140 protein levels were decreased in human colon cancers compared with those in normal mucosal tissue, and low levels of RIP140 expression in adenocarcinomas from patients correlated with poor prognosis. Together, these results support a tumor suppressor role for RIP140 in colon cancer.

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Section: Introductionmentioning

confidence: 99%

RIP140 increases APC expression and controls intestinal homeostasis and tumorigenesis

Lapierre¹,

Bonnet²,

Bascoul-Mollevi³

et al. 2014

J. Clin. Invest.

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“…Initially, it was isolated as an estrogen receptor α partner, though it interacts with many other NRs (Augereau et al 2006a). It consists of 1,158 amino acids in human and 1,161 amino acids in mouse, with 83% homology between the two sequences.…”

Section: Introductionmentioning

confidence: 99%

Tissue-specific expression of receptor-interacting protein in aging mouse

Ghosh

Thakur

2008

AGE

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Receptor-interacting protein (RIP) is a wellcharacterized coregulator for nuclear receptors. Here, we report the expression of RIP as two isoforms with molecular weights of 140 kDa and 137 kDa in liver and kidney, but only as one isoform of 140 kDa in lung, adipose tissue, prostate and testis of mice. The levels of both the isoforms decreased in liver and kidney of old mice compared with adult mice. The expression of RIP140 in kidney was relatively lower in old males than females. In contrast, adipose tissue showed remarkably higher levels of RIP140 in old than adult mice of both sexes. Thus, the expression of RIP varied with the type of tissue, sex and age of mice, suggesting differences in its function as a coregulator.

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“…Our work is mainly focused on RIP140 (receptor-interacting protein of 140 kDa, also known as NRIP1), a nuclear protein of 1,158 amino acids, initially identified as a transcription cofactor of estrogen receptors and shown to regulate energy homeostasis in metabolic tissues (see ref. 8 for a review). RIP140 is an atypical coregulator because, despite its recruitment by agonist-liganded nuclear receptors, it exhibits a strong transcriptional repressive activity.…”

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confidence: 99%

The Transcriptional Coregulator RIP140 Represses E2F1 Activity and Discriminates Breast Cancer Subtypes

Docquier

Harmand

Fritsch

et al. 2010

Clinical Cancer Research

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Purpose: Receptor-interacting protein of 140 kDa (RIP140) is a transcriptional cofactor for nuclear receptors involved in reproduction and energy homeostasis. Our aim was to investigate its role in the regulation of E2F1 activity and target genes both in breast cancer cell lines and in tumor biopsies.Experimental Design: Glutathione S-transferase pull-down assays, coimmunoprecipitation experiments, and chromatin immunoprecipitation analysis were used to evidence interaction between RIP140 and E2F1. The effects of RIP140 expression on E2F1 activity were determined using transient transfection and quantification of E2F target mRNAs by quantitative real-time PCR. The effect on cell cycle was assessed by fluorescence-activated cell sorting analysis on cells overexpressing green fluorescent protein-tagged RIP140. A tumor microarray data set was used to investigate the expression of RIP140 and E2F1 target genes in 170 breast cancer patients.Results: We first evidenced the complex interaction between RIP140 and E2F1 and showed that RIP140 represses E2F1 transactivation on various transiently transfected E2F target promoters and inhibits the expression of several E2F1 target genes (such as CCNE1 and CCNB2). In agreement with a role for RIP140 in the control of E2F activity, we show that increasing RIP140 levels results in a reduction in the proportion of cells in S phase in various human cell lines. Finally, analysis of human breast cancers shows that low RIP140 mRNA expression was associated with high E2F1 target gene levels and basal-like tumors.Conclusion: This study shows that RIP140 is a regulator of the E2F pathway, which discriminates luminal-and basal-like tumors, emphasizing the importance of these regulations for a clinical cancer phenotype. Clin Cancer Res; 16(11); 2959-70. ©2010 AACR.Cell cycle control is a fundamental process that governs cell proliferation and is frequently altered during tumorigenesis. E2Fs and their heterodimer partners (DP) are central regulators of cell cycle progression and directly regulate the expression of a broad spectrum of genes involved, for instance, in cell cycle regulation, DNA replication and repair, apoptosis, differentiation, or development (1, 2).E2F1, which was discovered as a protein promoting the transition to S phase, was the founding member of the E2F family, which comprises eight members in mammals. Among this family, some were initially presented as "activator E2Fs" (E2F1, E2F2, and E2F3), whereas the other members were mostly known as transcription repressors, although this classification now seemed too simplistic (reviewed in ref. 2 and references therein). E2F transcriptional activity was shown to be regulated by a large number of coactivators or corepressors, including the so-called pocket proteins, which form the retinoblastoma (RB) tumor suppressor family (pRB, together with the related proteins p107 and p130; ref. 3). RB attenuates E2F action by recruiting transcriptional corepressors such as histone deacetylases to E2F-regulated promoters, thus med...

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The nuclear receptor transcriptional coregulator RIP140

Cited by 51 publications

References 75 publications

RIP140 increases APC expression and controls intestinal homeostasis and tumorigenesis

RIP140 increases APC expression and controls intestinal homeostasis and tumorigenesis

Tissue-specific expression of receptor-interacting protein in aging mouse

The Transcriptional Coregulator RIP140 Represses E2F1 Activity and Discriminates Breast Cancer Subtypes

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