Fig. 7.

lncRNA MNX1-AS1 suppresses BTG2 transcription by binding to EZH2. a FISH and subcellular fractionation assays were used to determine the distribution of lncRNA MNX1-AS1 in SGC7901 and MGC803 cells. b Bioinformatics analysis was used to predict RBPs interacting with MNX1-AS1. c The RIP assays revealed the fold enrichment of MNX1-AS1 in EZH2/SUZ12/AGO2 RIP, as compared with its matched IgG control. d EZH2 was significantly decreased in GC cells transfected with EZH2 shRNA compared with scrambled group. e MTT assays were conducted to test the effects of EZH2 dwonregulation on GC cell viability. f EZH2 knockdown could obviously increase BTG2 expression in SGC7901 and MGC803 cells. g ChIP–qPCR analysis of EZH2 occupancy and H3K27me3 binding on the BTG2 promoter region after knockdown of MNX1-AS1 in SGC7901 and MGC803 cells. IgG was used as a negative control. h, i The promotion of GC proliferation, migration and invasion was partially reversed by overexpressing BTG2 expression in MGC803 cells