Truncated serine/arginine-rich splicing factor 3 accelerates cell growth through up-regulating c-Jun expression

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Author(s)

    • Kano Shizuka
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School|Student Lab, the University of Tokushima Faculty of Medicine
    • Rokutan Kazuhito
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
    • Nishida Kensei
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
    • Akaike Yoko
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
    • Kajita Keisuke
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
    • Kurokawa Ken
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
    • Masuda Kiyoshi
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
    • Kuwano Yuki
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
    • Tanahashi Toshihito
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School

Abstract

Serine/arginine-rich splicing factor 3 (SRSF3), a member of the SRSF family, plays a wide-ranging role in gene expression. The human <I>SRSF3</I> gene generates a major mRNA isoform encoding a functional, full-length protein and a PTC-containing isoform (<I>SRSF3-PTC</I>). The latter is expected to be degraded through the nonsense-mediated mRNA decay system. However, it was reported that <I>SRSF3-PTC</I> mRNA was produced under stressful conditions and translated into a truncated SRSF3 protein (SRSF3-TR). To disclose unknown functions of SRSF3-TR, we established Flp-In-293 cells stably expressing SRSF3-TR. The SRSF3-TR-expressing cells increased mRNA and protein levels of positive regulators for G1 to S phase transition (cyclin D1, cyclin D3, CDC25A, and E2F1) and accelerated their growth. c-Jun is required for progression through the G1 phase, the mechanism by which involves transcriptional control of the <I>cyclin D1</I> gene. We also found that the <I>JUN</I> promoter activity was significantly increased in the Flp-In-293 cells stably expressing SRSF3-TR, compared with mock-transfected control cells. The SRSF3-TR-expressing cells increased c-Jun and Sp-1 levels, which are important for the positive autoregulation and basal transcription of <I>JUN</I>, respectively. Our results suggest that stress-inducible SRSF3-TR may participate in the acceleration of cell growth through facilitating c-Jun-mediated G1 progression under stressful conditions. J. Med. Invest. 60: 228-235, August, 2013

Journal

  • The Journal of Medical Investigation

    The Journal of Medical Investigation 60(3.4), 228-235, 2013

    The University of Tokushima Faculty of Medicine

Codes

  • NII Article ID (NAID)
    130004822687
  • NII NACSIS-CAT ID (NCID)
    AA11166929
  • Text Lang
    ENG
  • Article Type
    journal article
  • ISSN
    1343-1420
  • Data Source
    IR  J-STAGE 
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