國家衛生研究院 NHRI:Item 3990099045/11621
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    题名: IGF-1 upregulates Survivin expression through PI-3K and CK2 pathways to inhibit 5-Fu induced apoptosis in esophageal carcinoma cells
    作者: Wong, FH;Juan, HC;Tsai, HT;Huang, CYF
    贡献者: Institute of Molecular and Genomic Medicine
    摘要: Insulin-like growth factor 1 (IGF-1) is a pleitrophic cytokine that not only regulates growth and differentiation of many cell types but also prevents apoptosis induced by various stimulations. In this study we investigated the effect of IGF-1 on Survivin expression in human esophageal carcinoma cells (CE cells). IGF-1 significantly inhibited apoptosis induced by 5-fluorouracil (5-Fu) and increased the expression of Survivin but had no effect on the expression of Bcl-2 and Bax. Over-expression of survivin using replication-deficient adenovirus increased cell survival from apoptosis induced by 5-Fu in CE cells. Adversely, using antisense-survivin to disrupt survivin expression, apoptosis induced by 5-Fu was significantly elevated and the protective effect of IGF-1 was significantly blocked. Our data indicated that IGF-1 inhibited 5-Fu induced apoptosis by increasing Survivin expression in CE cells. Furthermore, we demonstrated that IGF-1 regulated Survivin expression through PI 3-K and CK2 pathways. Our data indicated that the anti-apoptotic effect of IGF-1 was mediated by PI-3K and CK2 dependent up-regulation of Survivin in CE cells.
    日期: 2006-04
    關聯: Cancer Research. 2006 Apr;66(8, Suppl.):186.
    Link to: http://cancerres.aacrjournals.org/content/66/8_Supplement/186.4
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0008-5472&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000454606201444
    显示于类别:[黃奇英(1998-2005)] 會議論文/會議摘要

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