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RRM2 computational phosphoprotein network construction and analysis between no-tumor hepatitis/cirrhotic liver tissues and human hepatocellular carcinoma (HCC)

RRM2 computational phosphoprotein network construction and analysis between no-tumor hepatitis/cirrhotic liver tissues and human hepatocellular carcinoma (HCC)

Cellular Physiology and Biochemistry 26(3): 303-310

RRM2 computational phosphoprotein network construction and analysis of human hepatocellular carcinoma (HCC) is very useful to identify novel markers and potential targets for prognosis and therapy. By integration of gene regulatory network infer (GRNInfer) and the database for annotation, visualization and integrated discovery (DAVID) we identified and constructed significant molecule RRM2 phosphoprotein network from 25 no-tumor hepatitis/cirrhotic liver tissues and 25 HCC patients in the same GEO Dataset GSE10140-10141. We gained the negative result of RRM2 phosphoprotein module through the net numbers of activation minus inhibition compared with no-tumor hepatitis/cirrhotic liver tissues and predicted possibly the decrease of RRM2 phosphoprotein module in HCC. Our integrative result showed that RRM2 phosphoprotein cluster of HCC contained both in human no-tumor hepatitis/cirrhotic liver tissues and HCC terms of phosphoprotein (with RRM2) and cell cycle (without RRM2), only in HCC terms of cell-cell signaling, cell projection part, glycoprotein, cell projection, cell adhesion, biological adhesion, integral to plasma membrane, plasma membrane, kinase and phosphorus metabolic process (without RRM2), and none in HCC terms of cell death (without RRM2) and ion binding (with RRM2) compared with human no-tumor hepatitis/cirrhotic liver tissues, all the condition is vital to invasion of HCC. Therefore, we deduced the weaker RRM2 phosphoprotein function in HCC consistent with our above computation. It would be necessary of RRM2 phosphoprotein function decrease to invasion of HCC. RRM2 phosphoprotein interaction module construction in HCC can be a new route for studying the pathogenesis of HCC.

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Accession: 055338667

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PMID: 20798514

DOI: 10.1159/000320553

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