Serine/arginine-rich splicing factor 7 regulates p21-dependent growth arrest in colon cancer cells

• DOI: 10.2152/jmi.63.219
• Publication Date: 2016-09-16T18:08:24Z
• Authors: Saki Saijo; Yuki Kuwano; Kiyoshi Masuda; Tatsuya Nishikawa; Kazuhito Rokutan; Kensei Nishida
• Keywords: Splicing factor

Serine/arginine-rich splicing factors (SRSFs) play wide-ranging roles in gene expression through post-transcriptional regulation as well pre-mRNA splicing. SRSF7 was highly expressed colon cancer tissues, and its knockdown inhibited cell growth cells (HCT116) association with altered of 4,499 genes. The Ingenuity Pathway Analysis revealed that cycle-related canonical pathways were ranked the enriched category affected Western blotting confirmed p21, a master regulator cycle, increased without any induction p53 cells. Furthermore, cyclin-dependent kinase 2 retinoblastoma protein remained hypophosphorylated state. In addition, knockdown-induced inhibition observed p53-null HCT116 cells, suggesting p53-independent involved inhibition. reduction stabilized inhibitor 1A (CDKN1A) mRNA activation CDKN1A promoter. Interestingly, also blocked p21 degradation. These results suggest post-transcriptionally regulates at multistep processes. Thus, present findings disclose novel, important role proliferation regulating levels. J. Med. Invest. 63: 219-226, August, 2016.