CCNB1and CCNA2Activatory&Repressive Transition Mechanisms Between Human Normal Adjacent Tissues And Lung Adenocarcinoma

The aim of the paper is to understand cyclin B1(CCNB1)-mediated immune response and cell cycle, cyclinA2(CCNA2)-mediated cell division and autoimmunity activatory&repressive transition mechanisms between human normal adjacent tissues and lung adenocarcinoma. We recognized CCNB1and CCNA2-activatory different complete (all no positive correlation, Pearson CC<0.25) and uncomplete (partly no positive correlation besides CCNB1and CCNA2, Pearson CC0.25) networks in the lower human normal adjacent tissues and the higher lung adenocarcinoma through the corresponding CCNB1and CCNA2-stimulated (Pearson CC^0.25) or repressive (Pearson CC≤-0.25) overlapping molecules by means of Pearson and GRNInfer, respectively. The corresponding scatter matrix verified this result. Through the integrative analysis visualization caused by GO, KEGG, GenMAPP, BioCarta and disease database, the paper showed the results as follows:CCNB1-activatory different complete network was participated in acting matrix dipeptidyl-peptidase to doublecortin-like kinase and major histocompatibility complex class Ⅰ-induced immune response, whereas the corresponding repressive network participated in CCNB1repression with motor neuron and pancreas homeobox and E2F transcription factor to gamma-glutamyl cyclotransferase-induced cell cycle in lower human normal adjacent tissues.CCNB1-stimulated different complete network contained CCNB1 activation with desmoplakin to baculoviral IAP repeat, NIMA kinase and transforming acidic coiled-coil to endonuclease-induced cell cycle, whereas the corresponding repressive different complete network included CCNB1repression with collagen and WAP four-disulfide core to glucose/fructose transporter and ectodermal-neural cortex-induced immune response in higher lung adenocarcinoma.CCNA2-activatory different complete network was involved in CCNA2activation with LY6/PLAUR domain and docking protein, X antigen to solute neurotransmitter transporter, histone cluster-induced autoimmunity, whereas the corresponding repressive network participated in CCNA2repression with nucleus-localized protein binding dCTP pyrophosphatase1, cyclin E2and SAC3domain containing1-induced cell division in lower human normal adjacent tissues.CCNA2-stimulated different complete network contained CCNA2activation with desmoplakin, kinesin, non-SMC condensin, budding uninhibited by benzimidazoles, myeloblastosis viral oncogene-induced cell division, whereas the corresponding repressive different complete network included CCNA2repression with matrix-localized dipeptidyl-peptidase4and hyaluronan binding protein2to transmembrane protein63A-induced autoimmunity in higher lung adenocarcinoma.CCNB1and CCNA2different networks were confirmed by CCNB1and CCNA2-activatory or-repressive complete and uncomplete networks within and between human normal adjacent tissues or (and) lung adenocarcinoma.