| |
| We data-analyzed and constructed the high-expression GDPD5 immune inflammation-mediated angiogenesis and invasion regulation network in human hepatocellular carcinoma (HCC) compared with low-expression (fold change≥2) no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) in GEO data set, by using integration of gene regulatory network inference method with gene ontology (GO). Our result showed that GDPD5 immune inflammation and multi-regulation upstream network BIRC5, BRCA1, CDKN3, EYA1, HOXD4, LEF1, PLA2G1B, PROK1, PTHLH, ROBO1, SCML2, REG3A activated GDPD5, and downstream GDPD5-activated CAD, CDC2, CDKN3, DKK1, E2F1, FOXM1, HMGB2, MAP2, MYCN, MYH6, NEK2, NR5A1, PROK1 in HCC. We proposed that GDPD5 activated network enhanced blood coagulation, chemotaxis, inflammatory response, interleukin-8 production, leukocyte migration, neutrophil chemotaxis, neutrophil mediated immunity, receptor mediated endocytosis, positive regulation of DNA repair, positive regulation of protein ubiquitination, as a result of inducing immune inflammation-mediated angiogenesis and invasion regulation in HCC. Our hypothesis was verified by GDPD5 regulation subnetwork containing angiogenesis, cell proliferation, transcription from RNA polymerase II promoter, transcription from RNA polymerase III promoter, Wnt receptor signaling pathway; also by GDPD5 negative regulation subnetwork including centriole replication, fatty acid biosynthesis, transcription, cell-cell adhesion, microtubule depolymerization in HCC, respectively. |
|
| Keywords:GDPD5; human hepatocellular carcinoma (HCC); immune inflammation-mediated angiogenesis and invasion regulation network; biocomputation |
|
