國家衛生研究院 NHRI:Item 3990099045/11621

NHRI > Institute of Molecular and Genomic Medicine > Chi-Ying F. Huang(1998-2005) > Conference Papers/Meeting Abstract > Item 3990099045/11621

Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/11621

Title:	IGF-1 upregulates Survivin expression through PI-3K and CK2 pathways to inhibit 5-Fu induced apoptosis in esophageal carcinoma cells
Authors:	Wong, FH;Juan, HC;Tsai, HT;Huang, CYF
Contributors:	Institute of Molecular and Genomic Medicine
Abstract:	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.
Date:	2006-04
Relation:	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
Appears in Collections:	[Chi-Ying F. Huang(1998-2005)] Conference Papers/Meeting Abstract

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