Low And High EGRF₁ Activate Cell Cycle And Motility But Inhibit Growth And Development Different Mechanisms Between Human Normal Adjacent Tissues And Lung Adenocarcinoma

In this thesis,we aim to study that low and high EGFR₁ activate cell cycle and motility but inhibit cell growth and development different mechanisms between human normal adjacent tissues and lung adenocarcinoma.500 significant molecules were identified from 22,284 genes of 25 low human normal adjacent tissues compared with 25 high lung adenocarcinoma in GEO data set GSE7670.?http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE7670?and were processed by a series of biologically methods.Then we used GRNInfer,GVedit tools to construct EGFR₁-activation and-inhibition molecular network.Our identified EGFR₁ outside-inside-out interactive molecular network showed AGR2?anterior gradient homolog 2?Xenopus laevis??,SCG5?secretogranin V?7B2 protein??,WFDC2?WAP four-disulfide core domain 2?,PPAP2C?phosphatidic acid phosphatase 2C?,CCNU?cyclin O?in low human normal adjacent tissues.We propose low EGFR₁ outside-inside-out interactive neuropeptide-induced regulation of cell cycle through AGR2-SCG5-WFDC2-PPAP2C-CCNU in human normal adjacent tissues.Our identified EGFR₁ feedback-inhibitive molecular network showed EEF1A2?eukaryotic translation elongation factor 1 alpha 2?,SFN₃?REX2 RNA exonuclease 2 homolog?S.cerevisiae??,DKFZp762E1312?Holliday junction recognition protein?,PLK1?polo-like kinase 1?Drosophila??in low human normal adjacent tissues.We propose low EGFR₁ feedback-inhibitive nucleus cell growth through EEF1A2-SFN₃-DKFZp762E1312-PLK1 in human normal adjacent tissues.Our identified EGFR₁ inside-out activated molecular network showed SLC2A1?solute carrier family 2?facilitated glucose transporter?member 1?,CCNB2?cyclin B2?,HMMR?hyaluronan-mediated motility receptor?RHAMM??,KIF11?kinesin family member 11?,NUSAP1₁?nucleolar and spindle associated protein 1?,PRC1?protein regulator of cytokinesis 1?,UBE2C?ubiquitin-conjugating enzyme E2C?in high lung adenocarcinoma.We propose high EGFR₁ inside-out activated inflammation-induced motility through SLC2A1-CCNB2-HMMR-KIF11-NUSAP1₁-PRC1-UBE2C in lung adenocarcinoma.Our identified EGFR₁ inhibited molecular network showed CD 180?CD 180 molecule?,TNFRSF17?tumor necrosis factor receptor superfamily member 17?,POU2AF1?POU class 2 associating factor 1?in high lung adenocarcinoma.We propose high EGFR₁ inhibited inflammatory immune-induced membrane development through CD180-TNFRSF17-POU2AF1 in lung adenocarcinoma.These conclusions were further studied and verified based on integrative GO,KEGG,GenMAPP,BioCarta and disease databases.