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      Reconstruction of nuclear receptor network reveals that NR2E3 is a novel upstream regulator of ESR1 in breast cancer

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          Abstract

          ESR1 is one of the most important transcription factors and therapeutic targets in breast cancer. By applying systems-level re-analysis of publicly available gene expression data, we uncovered a potential regulator of ESR1. We demonstrated that orphan nuclear receptor NR2E3 regulates ESR1 via direct binding to the ESR1 promoter with concomitant recruitment of PIAS3 to the promoter in breast cancer cells, and is essential for physiological cellular activity of ESR1 in estrogen receptor (ER)-positive breast cancer cells. Moreover, expression of NR2E3 was significantly associated with recurrence-free survival and a favourable response to tamoxifen treatment in women with ER-positive breast cancer. Our results provide mechanistic insights on the regulation of ESR1 by NR2E3 and the clinical relevance of NR2E3 in breast cancer.

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          Cluster analysis and display of genome-wide expression patterns.

          P. T. Spellman, P. O. Brown, D Botstein … (1998)
          A system of cluster analysis for genome-wide expression data from DNA microarray hybridization is described that uses standard statistical algorithms to arrange genes according to similarity in pattern of gene expression. The output is displayed graphically, conveying the clustering and the underlying expression data simultaneously in a form intuitive for biologists. We have found in the budding yeast Saccharomyces cerevisiae that clustering gene expression data groups together efficiently genes of known similar function, and we find a similar tendency in human data. Thus patterns seen in genome-wide expression experiments can be interpreted as indications of the status of cellular processes. Also, coexpression of genes of known function with poorly characterized or novel genes may provide a simple means of gaining leads to the functions of many genes for which information is not available currently.
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            The NCI60 human tumour cell line anticancer drug screen.

            Robert Shoemaker (2006)
            The US National Cancer Institute (NCI) 60 human tumour cell line anticancer drug screen (NCI60) was developed in the late 1980s as an in vitro drug-discovery tool intended to supplant the use of transplantable animal tumours in anticancer drug screening. This screening model was rapidly recognized as a rich source of information about the mechanisms of growth inhibition and tumour-cell kill. Recently, its role has changed to that of a service screen supporting the cancer research community. Here I review the development, use and productivity of the screen, highlighting several outcomes that have contributed to advances in cancer chemotherapy.
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              Feasibility of a high-flux anticancer drug screen using a diverse panel of cultured human tumor cell lines.

              A. Monks, D Scudiero, P Skehan … (1991)
              We describe here the development and implementation of a pilot-scale, in vitro, anticancer drug screen utilizing a panel of 60 human tumor cell lines organized into subpanels representing leukemia, melanoma, and cancers of the lung, colon, kidney, ovary, and central nervous system. The ultimate goal of this disease-oriented screen is to facilitate the discovery of new compounds with potential cell line-specific and/or subpanel-specific antitumor activity. In the current screening protocol, each cell line is inoculated onto microtiter plates, then preincubated for 24-28 hours. Subsequently, test agents are added in five 10-fold dilutions and the culture is incubated for an additional 48 hours. For each test agent, a dose-response profile is generated. End-point determinations of the cell viability or cell growth are performed by in situ fixation of cells, followed by staining with a protein-binding dye, sulforhodamine B (SRB). The SRB binds to the basic amino acids of cellular macromolecules; the solubilized stain is measured spectrophotometrically to determine relative cell growth or viability in treated and untreated cells. Following the pilot screening studies, a screening rate of 400 compounds per week has been consistently achieved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): EMBO Mol Med
                Journal ID (iso-abbrev): EMBO Mol Med
                Journal ID (publisher-id): emmm
                Title: EMBO Molecular Medicine
                Publisher: WILEY-VCH Verlag (Weinheim )
                ISSN (Print): 1757-4676
                ISSN (Electronic): 1757-4684
                Publication date (Print): January 2012
                Volume: 4
                Issue: 1
                Pages: 52-67
                Affiliations
                [1 ]simpleDepartment of Systems Biology, The University of Texas M. D. Anderson Cancer Center Houston, TX, USA
                [2 ]simpleInstitute of Biosciences and Technology, Texas A&M University Health Science Center Houston, TX, USA
                [3 ]simpleGynecologic Medical Oncology, The University of Texas M. D. Anderson Cancer Center Houston, TX, USA
                [4 ]simpleBreast Medical Oncology, The University of Texas M. D. Anderson Cancer Center Houston, TX, USA
                [5 ]simpleDepartment of Life Science, Division of Life and Pharmaceutical Sciences, Center for Cell Signaling and Drug Discovery Research, Ewha Woman's University Seoul, Korea
                [6 ]simpleDepartment of Veterinary Physiology and Pharmacology, Texas A&M University College Station, TX, USA
                Author notes
                * Corresponding author: Tel: +1 713 834 6154; Fax: +1 713 563 4235; E-mail: jlee@ 123456mdanderson.org
                [†]

                These authors contributed equally to this work.

                Article
                DOI: 10.1002/emmm.201100187
                PMC ID: 3376834
                PubMed ID: 22174013
                SO-VID: 03d9c543-d3f5-46e0-b81e-5279d3534396
                Copyright © Copyright © 2012 EMBO Molecular Medicine
                History
                Date received : 01 July 2011
                Date revision received : 17 October 2011
                Date accepted : 26 October 2011
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Molecular medicine
                Keywords: nuclear receptor,nr2e3,microarray,breast cancer,genomics
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: nuclear receptor, nr2e3, microarray, breast cancer, genomics

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