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CacyBP/SIP protein promotes proliferation and G1/S transition of human pancreatic cancer cells
Author(s) -
Chen Xiong,
Mo Ping,
Li Xiaohua,
Zheng Peichan,
Zhao Lina,
Xue Zengfu,
Ren Gui,
Han Guohong,
Wang Xin,
Fan Daiming
Publication year - 2011
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.20737
Subject(s) - pancreatic cancer , biology , carcinogenesis , cancer research , cyclin e , cancer cell , ubiquitin , retinoblastoma protein , cancer , microbiology and biotechnology , cell cycle , cyclin , biochemistry , genetics , gene
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. Mol. Carcinog. © 2011 Wiley‐Liss, Inc.
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