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      The critical roles of COUP-TFII in tumor progression and metastasis

      review-article
      Author(s): , ,
      Publication date (Electronic):
      Journal: Cell & Bioscience
      Publisher: BioMed Central

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          Abstract

          Chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) belongs to the steroid/thyroid hormone receptor superfamily. Extensive evidence has indicated that COUP-TFII plays a critical and indispensable role in cell-fate specification, organogenesis, angiogenesis, and metabolism as well as in a variety of diseases. Recent studies obtained from genetically engineered mouse models (GEM) and patient specimen analysis indicate that COUP-TFII is also important for tumor progression and metastasis. In this article, we will comprehensively review the oncogenic roles of COUP-TFII within the tumor microenvironment and tumor cells and delineate the mechanism by which COUP-TFII contributes to tumorigenesis. The applicability of current data to our understanding of the role of COUP-TFII in cancer and the potential therapeutic implications will also be discussed.

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          Anatomical profiling of nuclear receptor expression reveals a hierarchical transcriptional network.

          Angie L Bookout, Yangsik Jeong, Michael Downes … (2006)
          In multicellular organisms, the ability to regulate reproduction, development, and nutrient utilization coincided with the evolution of nuclear receptors (NRs), transcription factors that utilize lipophilic ligands to mediate their function. Studying the expression profile of NRs offers a simple, powerful way to obtain highly relational information about their physiologic functions as individual proteins and as a superfamily. We surveyed the expression of all 49 mouse NR mRNAs in 39 tissues, representing diverse anatomical systems. The resulting data set uncovers several NR clades whose patterns of expression indicate their ability to coordinate the transcriptional programs necessary to affect distinct physiologic pathways. Remarkably, this regulatory network divides along the following two physiologic paradigms: (1) reproduction, development, and growth and (2) nutrient uptake, metabolism, and excretion. These data reveal a hierarchical transcriptional circuitry that extends beyond individual tissues to form a meganetwork governing physiology on an organismal scale.
          Article 0 comments Cited 306 times – based on 0 reviews     Review now
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            Notch signalling limits angiogenic cell behaviour in developing zebrafish arteries.

            Arndt F. Siekmann, Nathan D Lawson (2007)
            Recent evidence indicates that growing blood-vessel sprouts consist of endothelial cells with distinct cell fates and behaviours; however, it is not clear what signals determine these sprout cell characteristics. Here we show that Notch signalling is necessary to restrict angiogenic cell behaviour to tip cells in developing segmental arteries in the zebrafish embryo. In the absence of the Notch signalling component Rbpsuh (recombining binding protein suppressor of hairless) we observed excessive sprouting of segmental arteries, whereas Notch activation suppresses angiogenesis. Through mosaic analysis we find that cells lacking Rbpsuh preferentially localize to the terminal position in developing sprouts. In contrast, cells in which Notch signalling has been activated are excluded from the tip-cell position. In vivo time-lapse analysis reveals that endothelial tip cells undergo a stereotypical pattern of proliferation and migration during sprouting. In the absence of Notch, nearly all sprouting endothelial cells exhibit tip-cell behaviour, leading to excessive numbers of cells within segmental arteries. Furthermore, we find that flt4 (fms-related tyrosine kinase 4, also called vegfr3) is expressed in segmental artery tip cells and becomes ectopically expressed throughout the sprout in the absence of Notch. Loss of flt4 can partially restore normal endothelial cell number in Rbpsuh-deficient segmental arteries. Finally, loss of the Notch ligand dll4 (delta-like 4) also leads to an increased number of endothelial cells within segmental arteries. Together, these studies indicate that proper specification of cell identity, position and behaviour in a developing blood-vessel sprout is required for normal angiogenesis, and implicate the Notch signalling pathway in this process.
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              The orphan nuclear receptor COUP-TFII is required for angiogenesis and heart development.

              Marcelo Pereira, Yihsuan S. Tsai, Y Qiu … (1999)
              The embryonic expression of COUP-TFII, an orphan nuclear receptor, suggests that it may participate in mesenchymal-epithelial interactions required for organogenesis. Targeted deletion of the COUP-TFII gene results in embryonic lethality with defects in angiogenesis and heart development. COUP-TFII mutants are defective in remodeling the primitive capillary plexus into large and small microcapillaries. In the COUP-TFII mutant heart, the atria and sinus venosus fail to develop past the primitive tube stage. Reciprocal interactions between the endothelium and the mesenchyme in the vascular system and heart are essential for normal development of these systems. In fact, the expression of Angiopoietin-1, a proangiogenic soluble factor thought to mediate the mesenchymal-endothelial interactions during heart development and vascular remodeling, is down-regulated in COUP-TFII mutants. This down-regulation suggests that COUP-TFII may be required for bidirectional signaling between the endothelial and mesenchymal compartments essential for proper angiogenesis and heart development.
              Article 0 comments Cited 103 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Jun Qin: qinjun@sibs.ac.cn
                Sophia Y Tsai: stsai@bcm.edu
                Ming-Jer Tsai: mtsai@bcm.edu
                Journal
                Journal ID (nlm-ta): Cell Biosci
                Journal ID (iso-abbrev): Cell Biosci
                Title: Cell & Bioscience
                Publisher: BioMed Central (London )
                ISSN (Electronic): 2045-3701
                Publication date (Electronic): 1 October 2014
                Publication date PMC-release: 1 October 2014
                Publication date Collection: 2014
                Volume: 4
                Issue: 1
                Electronic Location Identifier: 58
                Affiliations
                [ ]Department of Urology, Renji Hospital Shanghai Jiao Tong University School of Medicine, Shanghai, 200127 China
                [ ]Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, People’s Republic of China
                [ ]Shanghai JiaoTong University School of Medicine, Shanghai, People’s Republic of China
                [ ]Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030 USA
                [ ]Program in Developmental Biology, Baylor College of Medicine, Houston, TX USA
                Article
                Publisher ID: 186
                DOI: 10.1186/2045-3701-4-58
                PMC ID: 4201699
                SO-VID: 01bb4e01-52d7-4dc2-967f-48fbb4e51fb4
                Copyright © © Qin et al.; licensee BioMed Central Ltd. 2014
                License:

                This article is published under license to BioMed Central Ltd. 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.

                History
                Date received : 17 August 2014
                Date accepted : 9 September 2014
                Categories
                Subject: Review
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                issue-copyright-statement © The Author(s) 2014

                ScienceOpen disciplines: Cell biology
                Data availability:
                ScienceOpen disciplines: Cell biology

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