IGHD/BIK/EGFR/SPINK1/CCNA2-repressive mechanism in lung adenocarcinoma

Zusatztext

Different Pearson mutual-positive-correlation IGHD/BIK/EGFR/SPINK1/CCNA2-repressive molecular network was constructed from the overlapping of GRNInfer and Pearson under IGHD/BIK/EGFR/SPINK1/CCNA2 CC =-0.25 in high lung adenocarcinoma compared with low human normal adjacent tissues, respectively. We propose IGHD inhibited DNA damage-induced inside-out cell differentiation through ENO1-SLC22A18-RECQL4-SQSTM1-PYCRL; BIK inhibiting axon guidance-induced membrane motility through BCC3-LGR4-DPY19L1-LIMK1; EGFR inhibited inflammatory immune-induced membrane development through CD180-TNFRSF17-POU2AF1; SPINK1 outside-inside-out inhibitive axon induced apoptosis through BUB1B-CCNA2-NCAPG-HIST1H2BD; CCNA2 inhibiting hypoxia, T cell and endocrine-induced cytoplasm differentiation through DPP41-DPP43-SLC2A5-TMEM63A-ENC12 in high lung adenocarcinoma based on integrative GO, KEGG, GenMAPP, BioCarta and disease databases. They are very useful to develop a new route and identify novel markers and potential drugs for prognosis and therapy for studying the pathogenesis

Autorenportrait

Prof. Dr. Lin Wang has received her Ph.D in Klinik für Innere Medizin, Friedrich-Schiller-Universität Jena, Germany. Currently, she is working as Biomedical Center professor in Beijing University of Posts and Telecommunications (BUPT).

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