Survivin (BIRC5) cell cycle computational network in human no-tumor hepatitis/cirrhosis and hepatocellular carcinoma transformation

• Published in: Journal of cellular biochemistry Vol. 112; no. 5; pp. 1286 - 1294
• Main Authors: Wang, Lin, Huang, Juxiang, Jiang, Minghu, Sun, Lingjun
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.05.2011
• Subjects: Algorithms; Carcinoma, Hepatocellular - genetics; Carcinoma, Hepatocellular - metabolism; cell cycle; Cell Cycle - genetics; Cell Transformation, Neoplastic - genetics; Cell Transformation, Neoplastic - metabolism; Databases, Genetic; Gene Regulatory Networks; Hepatitis B - genetics; Hepatitis B - metabolism; Hepatitis B virus; Hepatitis C - genetics; Hepatitis C - metabolism; Hepatitis C virus; human hepatocellular carcinoma; Humans; Inhibitor of Apoptosis Proteins - genetics; Inhibitor of Apoptosis Proteins - metabolism; Liver Cirrhosis - genetics; Liver Cirrhosis - metabolism; Liver Neoplasms - genetics; Liver Neoplasms - metabolism; Models, Genetic; no-tumor hepatitis/cirrhosis; survivin (BIRC5) computational network
• ISSN: 0730-2312; 1097-4644; 1097-4644
• DOI: 10.1002/jcb.23030

Survivin (BIRC5) relationship with tumor is presented in several papers. However, how the molecular network and interpretation concerning BIRC5 cell cycle between no‐tumor hepatitis/cirrhosis and hepatocellular carcinoma (HCC) remains to be elucidated. Here, we constructed and analyzed significant higher expression gene BIRC5 activated and inhibited cell cycle network from HCC versus no‐tumor hepatitis/cirrhosis pateints (viral infection HCV or HBV) in GEO Dataset by combination of gene regulatory network inference method based on linear programming and decomposition procedure with the CapitalBio MAS 3.0 software based on the integration of public databases including Gene Ontology, KEGG, BioCarta, GenMapp, Intact, UniGene, OMIM, etc. Compared the same and different activated and inhibited BIRC5 network with GO analysis between no‐tumor hepatitis/cirrhosis and HCC, our result showed BIRC5 cell cycle network weaker transcription factor activity in both no‐tumor hepatitis/cirrhosis and HCC (1); stronger nucleus protein binding but weaker cytoplasm protein binding in no‐tumor hepatitis/cirrhosis (2); stronger cytoplasm protein phosphatase binding but weaker ubiquitin‐protein ligase activity in HCC (3). Therefore, we inferred BIRC5 cell cycle module less transcription from RNA polymerase II promoter in both no‐tumor hepatitis/cirrhosis and HCC (4). We deduced BIRC5 cell cycle module different from more mitosis but less complex‐dependent proteasomal ubiquitin‐dependent protein catabolism as a result increasing cell division and cell numbers in no‐tumor hepatitis/cirrhosis to more protein amino acid autophosphorylation but less negative regulation of ubiquitin ligase activity during mitotic cell cycle as a result increasing growth and cell volume in HCC (5). J. Cell. Biochem. 112: 1286–1294, 2011. © 2011 Wiley‐Liss, Inc.