EGFR₂ Feedback/up/downstream-inhibited Pathway Induces Human Lung Adenocarcinoma Innate,Adaptive Immune Response And Regulation Mechanism

EGFR 2 inhibitive pathway and function are not clear through the corresponding indirect feedback/up/downstream mechanism in human lung adenocarcinoma. EGFR 2 inhibitive direct pathway was constructed in human lung adenocarcinoma by GRNInfer based on 24 Pearson mutual positive correlation from CC <-0.25 molecules with EGFR 2. EGFR 2 inhibitive indirect molecular pathway includes feedback HLA_C1-IGKC₂-IL8₂ loop or IGLJ3₁ to IGHD-POU2AF1,upstream IL8₁ to IGHM₃-IGL₂-IFI6 three to MGC29506,downstream IL8₄ to both CPVL-TNFRSF17 to IGL₅-IGHG1by hypothesis driven. Based on DAVID, EGFR 2 inhibitive indirect gene name pathway was identified as feedback major histocompatibility complex, class I, C ?HLA-C? - immunoglobulin kappa constant ?IGKC?-C-X-C motif chemokine ligand 8 ?CXCL8? loop or immunoglobulin lambda joining 3 ?IGLJ3? to immunoglobulin heavy constant delta?IGHD?-POU class 2 associating factor 1 ?POU2AF1?; upstream C-X-C motif chemokine ligand 8 ?CXCL8? to immunoglobulin heavy constant mu ?IGHM? - immunoglobulin lambda locus ?IGL? — interferon,alpha-inducible protein 6 ?IFI6? three to marginal zone B and B1 cell specific protein ?MZB1?; downstream C-X-C motif chemokine ligand 8?CXCL8? to both carboxypeptidase, vitellogenic like ?CPVL? — tumor necrosis factor receptor superfamily member 17 ?TNFRSF17? to immunoglobulin lambda locus ?IGL? — immunoglobulin heavy constant gamma 1 ?G1m marker? ?IGHG1?. Hypothesis is proposed that EGFR 2 feedback outside-in pathway inhibits innate humoral immune response through intracellular antigen-chemokine ligand loop or extracellular immunoglobulin receptor until nucleus DNA binding; upstream membrane pathway inhibits regulation of humoral immune response through extracellular region chemokine to cell surface peptidoglycan binding-immunoglobulin-mitochondrion interferon inducible three to endoplasmic reticulum B1 cell; downstream inside-out pathway inhibits adaptive immune response through intracellular chemokine to both extracellular exosome carboxypeptidase-plasma membrane receptor in human lung adenocarcinoma. It will be very useful to develop a new route of identifying novel markers and potential drugs for prognosis and therapy of cancer.