Differential Differentiation- and Survival and Invasion-related T-/Hcadherin (CDH13) Computational Downstream Network from No-Tumor Hepatitis/Cirrhosis (HBV or HCV infection) to Human Hepatocellular Carcinoma (HCC) Malignant TransformationLin Wang1*, Haijing Wu2, Minghu Jiang1, Juxiang Huang1, Hong Lin1 and Haizhen Diao1
- *Corresponding Author:
- Lin Wang
Biomedical Center, School of Electronics Engineering
Beijing University of Posts and Telecommunications
Beijing, 100876, China
E-mail: [email protected]
Received date: July 10, 2011; Accepted date: April 24, 2012; Published date: April 30, 2012
Citation: Wang L, Wu H, Jiang M, Huang J, Lin H, et al. (2012) Differential Differentiation- and Survival and Invasion-related T-/H-cadherin (CDH13) Computational Downstream Network from No-Tumor Hepatitis/Cirrhosis (HBV or HCV infection) to Human Hepatocellular Carcinoma (HCC) Malignant Transformation. J Mol Biomark Diagn 2:127. doi:10.4172/2155-9929.1000127
Copyright: © 2012 Wang L, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
We constructed and analyzed the low-and high-expression (fold change ≥2) different-activated and -inhibited T-/H-cadherin (CDH13) downstream network from no-tumor hepatitis/cirrhosis (HBV or HCV infection) to HCC malignant transformation in GEO data set by integration of gene regulatory network inference method based on linear programming and decomposition procedure with GO database. Our results show that the low-expression CDH13 downstream network has the multi-activated and -inhibited molecular pattern in no-tumor hepatitis/cirrhosis, whereas high-expression CDH13 downstream mainly somewhat inhibited molecular connections but significant reduced network (fold ≥2) in HCC. We suppose that the low-expression CDH13 downstream network mainly activates cell differentiation cell adhesion, but inhibits nuclear chromosome, mitosis in no-tumor hepatitis/cirrhosis, whereas the high-expression CDH13 downstream network activates Rab-protein geranylgeranyltransferase activity, protein modification, but inhibits modification-dependent protein catabolism and nucleotide binding in HCC. We put forward hypothesis that low-expression CDH13 activates cadherin binding, homophilic cell adhesion, negative regulation of cell adhesion, positive regulation of calcium-mediated signaling, calcium-dependent cell-cell adhesion, positive regulation of cell-matrix adhesion, low density lipoprotein mediated signaling and inhibits regulation of endothelial cell proliferation, positive regulation of smooth muscle cell proliferation, keratinocyte proliferation, as a result of inducing differentiation in no-tumor hepatitis/cirrhosis, whereas high-expression CDH13 activates positive regulation of survival gene product activity, protein homodimerization activity, Rho protein signal transduction, Rac protein signal transduction, positive regulation of cell migration, sprouting angiogenesis, positive regulation of positive chemotaxis, epidermal growth factor receptor signaling pathway, endothelial cell migration, lamellipodium biogenesis, and inhibits regulation of endocytosis, caveola, as a result of inducing survival and invasion in HCC. Our inferences are consistent with different-activated and -inhibited CDH13 downstream network, GO database and literatures, respectively.