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

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  • 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
  • Nishida Kensei
    Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
  • Nishiyama Chihiro
    Student Lab, the University of Tokushima Faculty of Medicine
  • 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
  • Rokutan Kazuhito
    Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School

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Serine/arginine-rich splicing factor 3 (SRSF3), a member of the SRSF family, plays a wide-ranging role in gene expression. The human SRSF3 gene generates a major mRNA isoform encoding a functional, full-length protein and a PTC-containing isoform (SRSF3-PTC). The latter is expected to be degraded through the nonsense-mediated mRNA decay system. However, it was reported that SRSF3-PTC 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 cyclin D1 gene. We also found that the JUN 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 JUN, 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

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