BRCA1-mediated inflammation and growth activated & inhibited transition mechanisms between no-tumor...

To understand breast cancer 1 early onset (BRCA1)-mediated inflammation and growth activated and inhibited transition mechanisms between no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) and human hepatocellular carcinoma (HCC), BRCA1-activated different complete (all no positive correlation, Pearson correlation coefficient <0.25) and uncomplete (partly no positive correlation except BRCA1, Pearson <0.25) networks were identified in higher HCC compared with lower no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) from the corresponding BRCA1-stimulated (Pearson ≥0.25) or inhibited (Pearson ≤-0.25) overlapping molecules of Pearson and GRNInfer, respectively. This result was verified by the corresponding scatter matrix. As visualized by GO, KEGG, GenMAPP, BioCarta, and disease database integration, we proposed mainly that BRCA1-stimulated different complete network was involved in BRCA1 activation with integral to membrane killer cell lectin-like receptor C to nucleus interferon regulatory factor 5-induced inflammation, whereas the corresponding inhibited network participated in BRCA1 repression with matrix roundabout axon guidance receptor homolog 1 to plasma membrane versican-induced growth in lower no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection). However, BRCA1-stimulated network contained BRCA1 activation with endothelium-specific to lysosomal transmembrane and carbamoyl synthetase to tastin, histone cluster and cyclin-induced growth, whereas the corresponding inhibited different complete network included BRCA1 repression with ovalbumin, thyroid stimulating hormone beta and Hu antigen C to cytochrome P450 to transducin-induced inflammation in higher HCC. Our BRCA1 different networks were verified by BRCA1-activated or -inhibited complete and uncomplete networks within and between no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) or (and) HCC.