REVIEW Open Access Expression and role of RIP140/NRIP1 in chronic lymphocytic leukemia Marion Lapierre 1,2,3,4 , Audrey Castet-Nicolas 1,2,3,4,5 , Delphine Gitenay 1,2,3,4 , Stéphan Jalaguier 1,2,3,4 , Catherine Teyssier 1,2,3,4 , Caroline Bret 6,7,3 , Guillaume Cartron 8,9,3 , Jérôme Moreaux 6,7,3 and Vincent Cavaillès 1,2,3,4* Abstract RIP140 is a transcriptional coregulator, (also known as NRIP1), which finely tunes the activity of various transcription factors and plays very important physiological roles. Noticeably, the RIP140 gene has been implicated in the control of energy expenditure, behavior, cognition, mammary gland development and intestinal homeostasis. RIP140 is also involved in the regulation of various oncogenic signaling pathways and participates in the development and progression of solid tumors. During the past years, several papers have reported evidences linking RIP140 to hematologic malignancies. Among them, two recent studies with correlative data suggested that gene expression signatures including RIP140 can predict survival in chronic lymphocytic leukemia (CLL). This review aims to summarize the literature dealing with the expression of RIP140 in CLL and to explore the potential impact of this factor on transcription pathways which play key roles in this pathology. Keywords: Chronic lymphocytic leukemia, Cell signaling, RIP140/NRIP1, Prognosis marker Introduction Chronic lymphocytic leukemia Chronic lymphocytic leukemia (CLL) is the most common form of leukemia in Western countries and mainly affects elderly individuals. CLL is characterized by the accumula- tion of malignant mature B cells in bone marrow, blood and lymphoid tissues. The clinical course of CLL is ex- tremely heterogeneous, with many patients presenting an indolent disease, whereas others exhibit an aggressive pathology and require treatment [1,2]. The diagnosis of CLL is based on biological criteria in- cluding the presence of a chronic lymphocytosis (≥5.10 9 /L) with a typical phenotype characterized by a κ or λ light chain restriction, the co-expression of B cell markers (CD19, CD20, CD22 with a low density, CD23) with the CD5 antigen (in the absence of other pan-T cell markers) and the expression of additional markers like CD200 or CD43 [3]. These characteristics are also sufficient for the distinction between CLL and other mature B cell disorders such as prolymphocytic leukemia, hairy-cell leukemia, mantle-cell lymphoma, or other lymphomas that can mimic CLL. CLL has previously been considered as a single entity with a variable clinical course. Recently, there has been considerable progress in the identification of molecular and cellular markers that may predict disease progression in patients with CLL [2]. Particularly, mutational profiles of Ig genes and cytogenetic abnormalities have been dem- onstrated to display a strong prognostic value (see below). The transcription factor RIP140 The transcription cofactor RIP140 (receptor-interacting protein of 140 kDa), known as nuclear receptor-interacting protein 1 (NRIP1), was first identified in human breast cancer cells through its interaction with the estrogen receptor α [4]. RIP140 was also shown to interact with many other nuclear receptors and transcription factors (for a review see [5]). RIP140 mainly acts as a transcrip- tional repressor by means of four inhibitory domains (see Figure 1) that recruit histone deacetylases or C-terminal binding proteins [6,7]. Moreover, several post-translational modifications, such as sumoylation and acetylation, play important roles in controlling the subcellular location and repressive activity of RIP140 (for a review [8]). RIP140 is an ubiquitously expressed gene, located on chromosome * Correspondence: vincent.cavailles@inserm.fr 1 IRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier F-34298, France 2 INSERM, U1194, Montpellier F-34298, France Full list of author information is available at the end of the article JOURNAL OF HEMATOLOGY & ONCOLOGY © 2015 Lapierre et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Lapierre et al. Journal of Hematology & Oncology (2015) 8:20 DOI 10.1186/s13045-015-0116-6