Camk1Computational Functional Network Construction And Theoretical Analysis In Human Hepatoma Calculation

In this study, our aim is to study novel high expression activated CAMKl mechanism and construct gene regulatory network in HCC. We analyzed different biological processes and occurrence numbers between high expression (fold change≥2) activated CAMK1gene ontology (GO) network of human hepatocellular carcinoma and corresponding low expression activated GO network of no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection). Using the significant analysis of microarrays (SAM), we identify high expression molecules from GEO data set and construct the network by GRNInfer.First, We compute the different biological processes and occurrence numbers of activated high expression CAMK1GO network in HCC compared with the corresponding low expression activated GO network of no-tumor hepatitis/cirrhotic tissues, the same compared with the corresponding inhibited CAMK1GO network of no-tumor hepatitis/cirrhotic tissues, and the different with the corresponding inhibited GO network of HCC, respectively. Second, we extract and compute activated CAMK1corresponding function molecular network and numbers in HCC referring to the different activated CAMK1GO-molecular network of HCC compared with the corresponding activated GO-molecular network of no-tumor hepatitis/cirrhotic tissues. Third, we verify the gene regulatory network and construct the molecular networks in vasculogenesis; cell aging; negative regulation of cell growth; apoptosis; regulation of cell migration; increase cell volume; regulation of insulin secretion; respectively.Activated CAMKl upstream natural killer cell cytotoxicity-mediated androgen receptor coupling protein geranylgeranylation and carbohydrate metabolism to calcium ion-dependent exocytosis and potassium ion transport to proteolysis-induced vasculogenesis network included BRCA1, RABGGTA, MAN2A1, STX1A, KCNQ3, PRSS1, NKX2-5in HCC; Activated CAMK1upstream negative regulation of EGFR, Wnt, MAPK, lipoprotein lipase and fatty acid biosynthesis-induced cell aging network included DKK1, NUP62, SORT1, BRCA1in HCC; Activated CAMK1downstream leukocyte migration-mediated Wnt receptor and phosphoinositide signal coupling protein ubiquitination to steroid metabolism-induced induction of apoptosis network included SFRP4, UBE2C, AKR1B10, CDKN2C in HCC; Activated CAMK1downstream regulation of protein metabolism-induced regulation of cell migration network included NTN1, UBE2C in HCC; Activated CAMK1downstream negative regulation of phosphorylation-induced negative regulation of cell growth network included CDKN2C in HCC; Activated CAMK1feedback G1/S transition of mitotic cell cycle-induced the increase cell volume network included CDKN3, CDKN2C in HCC; Activated CAMK1feedback activation of MAPK coupled to cyclic nucleotide second messenger-induced regulation of insulin secretion network included PROK1, SSTR5, MAP2K6, STX1A in HCC.