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ID 110162
著者
サイジョウ, サキ Department of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School.
桑野, 由紀 Department of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School. 徳島大学 教育研究者総覧 KAKEN研究者をさがす
増田, 清士 Department of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School. KAKEN研究者をさがす
西川, 達哉 Department of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School.
六反, 一仁 Department of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School. 徳島大学 教育研究者総覧 KAKEN研究者をさがす
西田, 憲生 Department of Pathophysiology, Institute of Biomedical Sciences, Tokushima University Graduate School. 徳島大学 教育研究者総覧 KAKEN研究者をさがす
キーワード
SRSF7
cell cycle
p21
G1/S arrest
資料タイプ
学術雑誌論文
抄録
Serine/arginine-rich splicing factors (SRSFs) play wide-ranging roles in gene expression through post-transcriptional regulation as well as pre-mRNA splicing. SRSF7 was highly expressed in colon cancer tissues, and its knockdown inhibited cell growth in colon cancer cells (HCT116) in association with altered expression of 4,499 genes. The Ingenuity Pathway Analysis revealed that cell cycle-related canonical pathways were ranked as the highly enriched category in the affected genes. Western blotting confirmed that p21, a master regulator in cell cycle, was increased without any induction of p53 in SRSF7 knockdown cells. Furthermore, cyclin-dependent kinase 2 and retinoblastoma protein were remained in the hypophosphorylated state. In addition, the SRSF7 knockdown-induced cell growth inhibition was observed in p53-null HCT116 cells, suggesting that p53-independent pathways were involved in the SRSF7 knockdown-induced cell growth inhibition. The reduction of SRSF7 stabilized cyclin-dependent kinase inhibitor 1A (CDKN1A) mRNA without any activation of the CDKN1A promoter. Interestingly, SRSF7 knockdown also blocked p21 degradation. These results suggest that the reduction of SRSF7 post-transcriptionally regulates p21 induction at the multistep processes. Thus, the present findings disclose a novel, important role of SRSF7 in cell proliferation through regulating p21 levels.
掲載誌名
The journal of medical investigation : JMI
ISSN
13431420
cat書誌ID
AA11166929
63
3-4
開始ページ
219
終了ページ
226
並び順
219
発行日
2016-08
EDB ID
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
医学系