Objective:To analyze the effects of cytomegalovirus (CMV) infection on gene expression and signaling pathways in preauricular somatic cells, and to explore potential intervention approaches for neonatal hearing loss caused by CMV infection.Methods:CMV infection data (GSE234062) were retrieved and downloaded from the GEO database. R studio software was used to analyze the differentially expressed genes (DEGs) between the CMV-infected group and the control group. ExpressAnalyst and String tools were employed to analyze the enrichment of DEGs in signaling pathways, biological processes, molecular functions, and protein-protein interactions.Results:After CMV infection of preauricular somatic cells, the expression levels of viral RNA and green fluorescent protein (GFP) RNA increased significantly. Meanwhile, 233 genes were upregulated and 123 genes were downregulated post-infection. Signaling pathway analysis showed that the upregulated genes were mainly enriched in pathways such as calcium ion channels, GABA synapses, morphine addiction, and cGMP-PKG, while the downregulated genes were primarily enriched in pathways including focal adhesion, extracellular matrix (ECM)-receptor interaction, amebiasis, and proteoglycans in cancer. Biological process analysis revealed that the upregulated genes were closely associated with neuron development and cell maturation, whereas the downregulated genes were mainly involved in actin filament-dependent processes, tissue development, and vascular development. Molecular function enrichment analysis indicated that the upregulated genes were mainly clustered in sequence-specific DNA binding, RNA polymerase Ⅱ distal enhancer binding, and G protein-coupled amine receptor activity, while the downregulated genes were closely related to molecular functions such as actin binding, structural molecule activity, and extracellular matrix structure.Conclusions:CMV infection can activate calcium ion channel and GABA synaptic pathways, and impair focal adhesion and ECM-receptor interaction pathways in preauricular somatic cells. This suggests that targeting these related pathways may help alleviate neonatal hearing impairment caused by CMV infection.

Objective:To analyze the effects of cytomegalovirus (CMV) infection on gene expression and signaling pathways in preauricular somatic cells, and to explore potential intervention approaches for neonatal hearing loss caused by CMV infection.Methods:CMV infection data (GSE234062) were retrieved and downloaded from the GEO database. R studio software was used to analyze the differentially expressed genes (DEGs) between the CMV-infected group and the control group. ExpressAnalyst and String tools were employed to analyze the enrichment of DEGs in signaling pathways, biological processes, molecular functions, and protein-protein interactions.Results:After CMV infection of preauricular somatic cells, the expression levels of viral RNA and green fluorescent protein (GFP) RNA increased significantly. Meanwhile, 233 genes were upregulated and 123 genes were downregulated post-infection. Signaling pathway analysis showed that the upregulated genes were mainly enriched in pathways such as calcium ion channels, GABA synapses, morphine addiction, and cGMP-PKG, while the downregulated genes were primarily enriched in pathways including focal adhesion, extracellular matrix (ECM)-receptor interaction, amebiasis, and proteoglycans in cancer. Biological process analysis revealed that the upregulated genes were closely associated with neuron development and cell maturation, whereas the downregulated genes were mainly involved in actin filament-dependent processes, tissue development, and vascular development. Molecular function enrichment analysis indicated that the upregulated genes were mainly clustered in sequence-specific DNA binding, RNA polymerase Ⅱ distal enhancer binding, and G protein-coupled amine receptor activity, while the downregulated genes were closely related to molecular functions such as actin binding, structural molecule activity, and extracellular matrix structure.Conclusions:CMV infection can activate calcium ion channel and GABA synaptic pathways, and impair focal adhesion and ECM-receptor interaction pathways in preauricular somatic cells. This suggests that targeting these related pathways may help alleviate neonatal hearing impairment caused by CMV infection.

Objective To find potential effective immunotherapy targets for acute myeloid leukemia (AML) by analyzing the expression and clinical significance of different immune checkpoints.Methods Gene expression profiles of AML cell lines (GSE57083) and tissues (GSE37642) were downloaded from GEO database.Then different immune checkpoints expression and clinical significance were analyzed with R studio and GraphPad software.Results In 16 AML cell lines,the expression rank of 11 immune checkpoints genes was LGALS9,PVRL2,PVR,PDCD1,TIM3,CTLA4,PDL1,GITR,LAG3,PDL2,GITRL,and among which LGALS9,PVRL2,GITR had larger variation between different cells.In AML tissues,the expression rank of immune checkpoint was LGALS9,PVRL2,TIM3,PDCD1,CTLA4,LAG3,GITR,PDL1,PVR,GITRL,PDL2.Survival analysis revealed high expression of PVR and LGALS9 was associated with poor prognosis,while the survival time had no significant difference in other genes.Conclusions PVR is highly expressed in AML tumor cells,and LGALS9 is highly expressed in both AML tumor cells and tissues.High expression of PVR and LGALS9 is associated with poor prognosis of AML patients,which may be a potential effective immunotherapy target for AML.

Objective: To explore potential therapeutic targets for neonatal hypoxic brain injury, we analyzed the effects of hypoxia on the gene expression profiles and signaling pathway in 3D cultured cerebral cortex cells. Methods: R studio software was used to analyze the differentially expressed genes of hypoxia treated cerebral cortex cell data (GSE112137) which was downloaded from GEO database. Gene Oncology and KEGG software were used to enrich the molecular function, biological process and signaling pathways of differentially expressed genes. Then String and Cytoscape software were adapted to analyzed gene interaction network between these genes. Results: There were 395 increasing genes and 185 decreasing genes (Change Fold≥2) were identified in hypoxic cerebral cells compared with the control groups. Most elevated genes were mainly related with molecular function including dioxygenase activity, isomerase activity and misfolded protein binding, while the decreasing genes were enriched in RNA polymerase Ⅱ proximal promoter sequence-specific DNA binding. Biological process enrichment analysis revealed that hypoxia up-regulated genes were associated with endoplasmic reticulum stress, oxidation-reduction process and glycolysis, while down-regulated genes were involved in the progress of neural development and cell differentiation. KEGG pathway enrichment results indicated hypoxia increasing genes were mainly related with endoplasmic reticulum protein processing, glycolysis, amino acid biosynthesis, and decreasing genes were mainly enriched in Parkinson′s disease signaling pathway. Conclusions Hypoxia in human cerebral cortex cells could cause endoplasmic reticulum stress, protein misfolding and metabolic abnormalities, inhibited the development of neuron cells. Drugs targeting these process may be beneficial to alleviate cerebral hypoxia injury.