title: BRCA1-mediated inflammation and growth activated & inhibited transition mechanisms between no-tumor hepatitis/cirrhotic tissues and HCC.
abstract: 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.
authors.affiliation: Bioinformatics Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, 100876, China; State key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
authors.forename: Haizhen
authors.initials: H
authors.lastname: Diao
authors.forename: Lin
authors.initials: L
authors.lastname: Wang
authors.forename: Juxiang
authors.initials: J
authors.lastname: Huang
authors.forename: Minghu
authors.initials: M
authors.lastname: Jiang
authors.forename: Huilei
authors.initials: H
authors.lastname: Zhou
authors.forename: Xiaohe
authors.initials: X
authors.lastname: Li
authors.forename: Qingchun
authors.initials: Q
authors.lastname: Chen
authors.forename: Zhenfu
authors.initials: Z
authors.lastname: Jiang
authors.forename: Haitao
authors.initials: H
authors.lastname: Feng
mesh_terms: D019313:BRCA1 Protein / Q000235:genetics / Q000378:metabolism*; D006528:Carcinoma, Hepatocellular / Q000378:metabolism* / Q000473:pathology; D053263:Gene Regulatory Networks; D006505:Hepatitis / Q000378:metabolism; D006509:Hepatitis B / Q000235:genetics / Q000378:metabolism*; D006526:Hepatitis C / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D008103:Liver Cirrhosis / Q000235:genetics / Q000378:metabolism*; D008113:Liver Neoplasms / Q000378:metabolism* / Q000473:pathology
chemical_list: D019313:BRCA1 Protein; C492913:BRCA1 protein, human; D018836:Inflammation Mediators
keywords: BREAST CANCER 1 EARLY ONSET (BRCA1); GROWTH; HCC; INFLAMMATION; NO-TUMOR HEPATITIS/CIRRHOTIC TISSUES (HBV OR HCV INFECTION)