CacyBP/SIP Protein Promotes Proliferation and G1/S Transition of Human Pancreatic Cancer Cells

被引：27
作者：
Chen, Xiong [1 ,2 ]
Mo, Ping [1 ,2 ]
Li, Xiaohua [1 ,2 ]
Zheng, Peichan [3 ]
Zhao, Lina [1 ,2 ]
Xue, Zengfu [1 ,2 ]
Ren, Gui [1 ,2 ]
Han, Guohong [1 ,2 ]
Wang, Xin [1 ,2 ]
Fan, Daiming [1 ,2 ]
机构：
[1] Fourth Mil Med Univ, State Key Lab Canc Biol, Xian 710032, Shaanxi, Peoples R China
[2] Fourth Mil Med Univ, Xijing Hosp Digest Dis, Xian 710032, Shaanxi, Peoples R China
[3] Peoples Hosp Fujian Prov, Dept Clin Lab, Fuzhou, Fujian, Peoples R China
来源：
MOLECULAR CARCINOGENESIS | 2011年 / 50卷 / 10期
基金：
中国国家自然科学基金;
关键词：
CacyBP/SIP; proliferation; cell cycle; pancreatic cancer; BINDING-PROTEIN; SIGNALING PATHWAY; CALCYCLIN; EXPRESSION; PROSTATE; APOPTOSIS; RECEPTOR; DIFFERENTIATION; TARGET; GROWTH;
D O I：
10.1002/mc.20737
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Calcyclin-binding protein or Siah-1-interacting protein (CacyBP/SIP), a component of the ubiquitin-mediated proteolysis, could participate in beta-catenin degradation, which was found to be related to the malignant phenotypes of pancreatic cancer previously. However, the role of CacyBP/SIP itself in pancreatic cancer has not been investigated. In the present study, CacyBP/SIP expression was assayed and manipulated to reveal the potential mechanism in pancreatic cancer carcinogenesis. Here, we show that CacyBP/SIP is over-expressed in pancreatic cancer cells. Down-regulation of CacyBP/SIP by small interference RNA (siRNA) severely suppresses the proliferation and tumorigenesis in pancreatic cancer. G1/S transition arrest induced by inhibition of CacyBP/SIP is at least partly mediated by down-regulation of Cyclin E and CDK2 as well as up-regulation of p27 and Rb. Collectively, CacyBP/SIP as an enhancer of pancreatic cancer malignance might develop into another possible therapeutic target. (C) 2011 Wiley-Liss, Inc.
引用
收藏
页码：804 / 811
页数：8
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