The Journal of Medical Investigation
Online ISSN : 1349-6867
Print ISSN : 1343-1420
ISSN-L : 1343-1420
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Truncated serine/arginine-rich splicing factor 3 accelerates cell growth through up-regulating c-Jun expression
Shizuka KanoKensei NishidaChihiro NishiyamaYoko AkaikeKeisuke KajitaKen KurokawaKiyoshi MasudaYuki KuwanoToshihito TanahashiKazuhito Rokutan
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2013 Volume 60 Issue 3.4 Pages 228-235

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Abstract

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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© 2013 by The University of Tokushima Faculty of Medicine
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