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Joint analysis of lncRNA m(6)A methylome and lncRNA/mRNA expression profiles in gastric cancer

BACKGROUND: N(6)-methyladenosine (m(6)A) modification might be closely associated with the genesis and development of gastric cancer (GC). Currently, the evidence established by high-throughput assay for GC-related m(6)A patterns based on long non-coding RNAs (lncRNAs) remains limited. Here, a joint...

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Detalles Bibliográficos
Autores principales: Lv, Zhi, Sun, Liping, Xu, Qian, Xing, Chengzhong, Yuan, Yuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7517696/
https://www.ncbi.nlm.nih.gov/pubmed/32982586
http://dx.doi.org/10.1186/s12935-020-01554-8
Descripción
Sumario:BACKGROUND: N(6)-methyladenosine (m(6)A) modification might be closely associated with the genesis and development of gastric cancer (GC). Currently, the evidence established by high-throughput assay for GC-related m(6)A patterns based on long non-coding RNAs (lncRNAs) remains limited. Here, a joint analysis of lncRNA m(6)A methylome and lncRNA/mRNA expression profiles in GC was performed to explore the regulatory roles of m(6)A modification in lncRNAs. METHODS: Three subjects with primary GC were enrolled in our study and paired sample was randomly selected from GC tissue and adjacent normal tissue for each case. Methylated RNA Immunoprecipitation NextGeneration Sequencing (MeRIP-Seq) and Microarray Gene Expression Profiling was subsequently performed. Then co-expression analysis and gene enrichment analysis were successively conducted. RESULTS: After data analysis, we identified 191 differentially m(6)A-methylated lncRNAs, 240 differentially expressed lncRNAs and 229 differentially expressed mRNAs in GC. Furthermore, four differentially m(6)A-methylated and expressed lncRNAs (dme-lncRNAs) were discovered including RASAL2-AS1, LINC00910, SNHG7 and LINC01105. Their potential target genes were explored by co-expression analysis. And gene enrichment analysis suggested that they might influence the cellular processes and biological behaviors involved in mitosis and cell cycle. The potential impacts of these targets on GC cells were further validated by CCLE database and literature review. CONCLUSIONS: Four novel dme-lncRNAs were identified in GC, which might exert regulatory roles on GC cell proliferation. The present study would provide clues for the lncRNA m(6)A methylation-based research on GC epigenetic etiology and pathogenesis.