AGR2Common And Different Activatory And Repressive Function And Mechanism Network In Human Lung Adenocarcinoma And Normal Adjacent Tissues

In this paper, to construct AGR2common and different activatory and repressive function and mechanism network in human lung adenocarcinoma and normal adjacent tissues. We provide a complete set of biomedical calculation system:Choosing omic data Using GEO database GSE7670, Selecting500significant high expression (Fold change≥2) molecule from human normal adjacent tissues comparing with lung adenocarcinoma from22284molecules of25human normal adjacent tissues and25lung adenocarcinoma samples with the method SAM. We establish3molecule net through computational biology related calculation and analysis.To study anterior gradient homolog2(AGR2)-activatory mechanism from hypoxia-induced inflammation to cell division, AGR2-activatory common complete (all positive CC (Pearson correlation coefficient)>0.25) and uncomplete (partly positive besides AGR2) networks were constructed between low and high lung adenocarcinoma from the corresponding Pearson (AGR2CC≥0.25) and GRNInfer overlapping molecules, and verified by Scatter Matrix, respectively. We proposed that AGR2-activatory hypoxia-induced inflammation’s common complete mechanism was involved in AGR2stimulation with plasma membrane carcinoma cluster antigen to cell junction to serine-type endopeptidase proteolysis in human normal adjacent tissues by integrative analysis of GO, KEGG, GenMAPP, BioCarta and disease database. However, AGR2-activatory cell division’s common complete mechanism participated in AGR2stimulation with Estrogen-responsive polyproline-specific translation elongation factor to transcription factor binding mitotic spindle checkpoint in lung adenocarcinoma.To study anterior gradient homolog2(AGR2)-activatorymechanism from humoral immune response to inflammation-associated cell cycle, AGR2-activatory different complete (all no positiveCC (Pearson correlation coefficient)<0.25) and uncomplete (partly no positive except AGR2) networks were constructed between low human normal adjacent tissues and high lung adenocarcinoma from the corresponding Pearson (AGR2CC≥0.25) and GRNInfer overlapping molecules,and verified via Scatter Matrix, respectively. We proposed that AGR2-activatory humoral immune response’s different complete mechanismwas involved in AGR2stimulation with matix cytokine and calcium ion binding to hypothetical protein FLJ22184in human normal adjacent tissues by integrative analysis of GO, KEGG, GenMAPP, BioCarta and disease database. However, AGR2-activatory inflammation-associated cell cycle’s different complete mechanism participated in AGR2stimulation with hyaluronan to endoplasmic reticulum intracellular protein transport to spindle microtubule binding baculoviral1AP repeat and kinesin microtubule-based and nonhistone chromosomal high-mobility to cell division cycle in lung adenocarcinoma.To study anterior gradient homolog2(AGR2)-mediated mechanism from T cell receptor signaling pathway to humoral immune response, AGR2-repressive different complete (all no positiveCC (Pearson correlation coefficient)<0.25) and uncomplete (partly no positive except AGR2) networks were constructed between low human normal adjacent tissues and high lung adenocarcinoma from the corresponding Pearson (AGR2CC≤-0.25) and GRNInfer overlapping molecules,and verified by Scatter Matrix, respectively. We proposed that AGR2-repressive T cell receptor signaling pathway’s different complete mechanism was involved in AGR2repression with calcium ion binding cell adhesion coupling protein kinase C and SH3domain to chromosome2open reading frame27in human normal adjacent tissues by integrative analysis of GO, KEGG, GenMAPP, BioCarta and disease database. However, AGR2-repressive humoral immune response’s different complete mechanism participated in AGR2repression with microtubule associated serine/threonine kinase activity establishment and/or maintenance of cell polarity to coactivator transcription from RNA polymerase Ⅱ promoter in lung adenocarcinoma.