BRCA1‐Mediated Inflammation and Growth Activated & Inhibited Transition Mechanisms Between No‐Tumor Hepatitis/Cirrhotic Tissues and HCC. Issue 4 (April 2014)

• Record Type: Journal Article
• Authors: Diao, Haizhen; Wang, Lin; Huang, Juxiang; Jiang, Minghu; Zhou, Huilei; Li, Xiaohe; Chen, Qingchun; Jiang, Zhenfu; Feng, Haitao
• Is Part Of: Journal of cellular biochemistry. Volume 115:Issue 4(2014:Apr.)
• Page Start: 641
• Page End: 650
• Publication Date: 2014-04
• Subjects: Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.24699
• Languages: English
• ISSNs: 0730-2312

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>ABSTRACT</title> <sec id="jcb24699-sec-0001" sec-type="section"> <p>To understand breast cancer 1 early onset (<italic>BRCA1</italic>)‐mediated inflammation and growth activated and inhibited transition mechanisms between no‐tumor hepatitis/cirrhotic tissues (HBV or HCV infection) and human hepatocellular carcinoma (HCC), <italic>BRCA1</italic>‐activated different complete (all no positive correlation, Pearson correlation coefficient <0.25) and uncomplete (partly no positive correlation except <italic>BRCA1</italic>, Pearson <0.25) networks were identified in higher HCC compared with lower no‐tumor hepatitis/cirrhotic tissues (HBV or HCV infection) from the corresponding <italic>BRCA1</italic>‐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 <italic>BRCA1</italic>‐stimulated different complete network was involved in <italic>BRCA1</italic> 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 <italic>BRCA1</italic> 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, <italic>BRCA1</italic>‐stimulated network contained <italic>BRCA1</italic> 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 <italic>BRCA1</italic> repression with ovalbumin, thyroid stimulating hormone beta and Hu antigen C to cytochrome P450 to transducin‐induced inflammation in higher HCC. Our <italic>BRCA1</italic> different networks were verified by <italic>BRCA1</italic>‐activated or ‐inhibited complete and uncomplete networks within and between no‐tumor hepatitis/cirrhotic tissues (HBV or HCV infection) or (and) HCC. J. Cell. Biochem. 115: 641–650, 2014. © 2013 Wiley Periodicals, Inc.</p> </sec> </abstract>