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Microarray analysis of genes with differential expression of m6A methylation in lung cancer

Authors
  • Wu, Shuo1
  • Lv, Xing1
  • Zhang, Yan1
  • Xu, Xi1
  • Zhao, Feng1
  • Zhang, Yao2
  • Chen, Lizhan2
  • ou-Yang, Haifeng2
  • Ti, Xinyu1
  • 1 Department of Pulmonary and Critical Care Medicine, Xijing Hospital, Fourth Military Medical University, Xi’an, Shanxi 710032, China
  • 2 Department of Pulmonary Medicine, Thoracis Hospital Xi’an International Medical Center, Xi’an, Shanxi 710100, China
Type
Published Article
Journal
Bioscience Reports
Publisher
Portland Press
Publication Date
Sep 17, 2021
Volume
41
Issue
9
Identifiers
DOI: 10.1042/BSR20210523
PMID: 34308964
PMCID: PMC8450313
Source
PubMed Central
Keywords
Disciplines
  • Research Articles
License
Unknown

Abstract

Purpose: N6-methyladenosine (m6A) is among the most abundant mRNA modifications in eukaryote. The aim of the present study was to investigate function of m6A mRNA methylation in lung cancer and the underlying mechanism. Methods: Microarray analysis was performed to detect the differences in RNA expression between cancerous and adjacent non-cancerous tissue samples. The target mRNAs were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Hierarchical clustering of RNAs was conducted to identify distinct m6A methylation or expression patterns between the samples. Results: In the present study, some differentially expressed genes (DEGs) of mRNAs were identified, including up-regulated secret phosphoprotein 1 (SPP1) and down-regulated pRB. Functional enrichment analysis revealed that while differential hypermethylation was related to cell cycle, intracellular part and protein binding, the main pathway involved herpes simplex virus 1 infection related to down-regulated AKT, Araf1 and BCL2A1. In the meantime, sexual reproduction, cohesin complex and protein C-terminus binding was functionally linked to differential hypomethylation, while fluid shear stress and atherosclerosis were identified as the main pathways related to up-regulated GST and CNP. Conclusions: We showed that lung cancer development involved differential expression of SPP1 and pRB mRNA, as well as m6A mRNA methylation in AKT, APAF1, BCL2A1, GST and CNP genes.

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