DNA methylation contributes to silencing the expression of linc00086 in gastric cancer.

Previous evidence has revealed that long non-coding RNAs serve important functions in numerous types of cancer when dysregulated, including in gastric cancer (GC). In the present study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis was used to detect the expression of small integral membrane protein 10 like 2A (linc00086) in GC tissues and non-cancerous tissues, and the expression of linc00086 in GC cell lines was analyzed. A RT-qPCR assay was used to assess linc00086 expression levels in GC cell lines following treatment with 5-Aza-2'-deoxycytidine (5-aza-dC), which is a DNA methyltransferase inhibitor. Small interfering RNA was used to silence the expression of methyl-CpG binding protein 2 (MeCP2), and then the expression of linc00086 was detected. Linc00086 expression was revealed to be downregulated in GC tissues and GC cell lines. Furthermore, it was revealed that 5-aza-dC induced linc00086 expression in SGC-7901 and MKN45 cells, and analysis of CpG methylation by bisulfite sequencing-polymerase chain reaction demonstrated that DNA methylation may regulate the expression of linc00086. MeCP2 is involved in gene regulation by binding to methylated promoters, and it was revealed that the knockdown of the expression of MeCP2 resulted in a higher expression of linc00086. The present study revealed that DNA methylation regulate the expression of linc00086 in human GC cell lines.