[No authors listed]
Hypermethylation of transcription factor activating enhancerâbinding protein 2e (TFAP2E) has been reported to be associated with chemoresistance to 5âfluorouracil (5âFU) in gastric cancer (GC). In the present study, the molecular mechanism governing this chemoresistance was investigated. Drugâresistant human GC MGCâ803/5âFU cells were established and TFAP2E expression and methylation levels were assessed. Autocrine exosomes from GC culture medium were isolated and characterized. MicroRNA (miRNA) microarray analysis was used to determine the miRNA expression profile of GC cellâderived exosomes. Exosomes collected from MGCâ803/5âFU cells were coâcultured with control cells, and 5âAzaâ2'âdeoxycytidine (5Aza) was added into MGCâ803/5âFU cells to investigate the relationship between TFAP2E, exosomes and chemosensitivity. In the present study, it was demonstrated that hypermethylation of TFAP2E resulted in its reduced expression and 5âFU chemoresistance in GC cells. miRNAs miRâ106aâ5p and miRâ421 were highly expressed and regulated the chemoresistance induced by TFAP2E methylation. Target gene prediction using miRBase, TargetScan and PicTar revealed that E2F1, MTOR and may be TFAP2E target genes in GC. Collectively, our data support an important role of exosomes and exosomal miRNAs in TFAP2E methylationâinduced chemoresistance to 5âFU in GC. These results highlight their potential for miRNAâbased therapeutics.
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