Journal of Cellular Biochemistry

BRCA1-Mediated Inflammation and Growth Activated & Inhibited Transition Mechanisms Between No-Tumor Hepatitis/Cirrhotic Tissues and HCC

Authors

  • Haizhen Diao,

    1. Bioinformatics Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, China
    2. State key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China
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  • Lin Wang,

    Corresponding author
    1. Bioinformatics Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, China
    2. State key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China
    • Correspondence to: Prof. Lin Wang, Bioinformatics Center, School of Electronics Engineering, Beijing University of Posts and Telecommunications, Beijing 100876, China.

      Email: wanglin98@tsinghua.org.cn

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  • Juxiang Huang,

    1. Bioinformatics Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, China
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  • Minghu Jiang,

    1. Lab of Computational Linguistics, School of Humanities and Social Sciences, Tsinghua University, Beijing, China
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  • Huilei Zhou,

    1. Bioinformatics Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, China
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  • Xiaohe Li,

    1. Bioinformatics Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, China
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  • Qingchun Chen,

    1. Bioinformatics Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, China
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  • Zhenfu Jiang,

    1. School of Mechanical Electronic & Information Engineering, China University of Mining & Technology, Beijing, China
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  • Haitao Feng

    1. Heilongjiang University of Chinese Medicine, Harbin, China
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  • Conflict of interest: None.
  • Haizhen Diao, Lin Wang, Juxiang Huang, and Minghu Jiang contributed equally to this work.

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. J. Cell. Biochem. 115: 641–650, 2014. © 2013 Wiley Periodicals, Inc.

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