title: SMC3 may play an important role in atopic asthma development.
abstract: BACKGROUND
  As a common disease with a complex risk, including genetic and environmental factors, atopic asthma is prevalent but treatable. The aim of the study was to predict the underlying mechanism of asthma and identify target genes for the disease.
  
  
  METHODS
  The affymetrix chip data, GSE18965, were available from Gene Expression Omnibus and the differentially expressed genes (DEGs) between nine atopic asthmatic specimens and seven healthy nonatopic samples were identified by R. Then Gene Ontology and pathway enrichment analyses were performed to these DEGs. Further, search tool for the retrieval of interacting genes/proteins (STRING) was used to select protein-protein interaction (PPI) for DEGs, and then the network was visualized by Cytoscape. Finally, transcription factor binding site analysis was conducted to the hot gene.
  
  
  RESULTS
  Total 565 DEGs were identified, including 535 upregulated and 30 downregulated genes. The upregulated genes, such as structural maintenance of chromosome (SMC)3, significantly affected cellular component of extracellular matrix (P = 1.56E-04). Otherwise, DEGs were remarkably enriched in three pathways, including transforming growth factor-beta signaling pathway (P = 0.005252649). Further, SMC3 was detected as hot gene in PPI network, and NET (Elk3) was predicted as the significant transcription factor for this gene.
  
  
  CONCLUSIONS
  SMC3 may play an important role in atopic asthma development; therefore, it has the potential to be the target for the disease. Moreover, our findings provide more knowledge about the mechanism of atopic asthma and help the researchers to explore it in future.
authors.affiliation: Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Cheng
authors.affiliation: Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
authors.forename: Wanjie
authors.initials: W
authors.lastname: Huang
authors.affiliation: Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
authors.forename: Ning
authors.initials: N
authors.lastname: Chen
authors.affiliation: Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
authors.forename: Yunxiao
authors.initials: Y
authors.lastname: Shang
authors.affiliation: Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
authors.forename: Han
authors.initials: H
authors.lastname: Zhang
mesh_terms: D000293:Adolescent; D001249:Asthma / Q000235:genetics* / Q000378:metabolism; D018797:Cell Cycle Proteins / Q000235:genetics* / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D011508:Chondroitin Sulfate Proteoglycans / Q000235:genetics* / Q000378:metabolism; D002868:Chromosomal Proteins, Non-Histone / Q000235:genetics* / Q000378:metabolism; D020869:Gene Expression Profiling / Q000379:methods; D020022:Genetic Predisposition to Disease; D006801:Humans; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods; D060066:Protein Interaction Maps; D055815:Young Adult
chemical_list: D018797:Cell Cycle Proteins; D011508:Chondroitin Sulfate Proteoglycans; D002868:Chromosomal Proteins, Non-Histone; C492318:SMC3 protein, human
keywords: asthma; differentially expressed genes; functional analysis; protein-protein interaction network; transcription factor binding site