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. 2019 Sep 20;11:8589–8602. doi: 10.2147/CMAR.S186002

Figure 6.

Figure 6

(A) The BGC-823 cells were treated with 5-azacytidine, and the expression level of KCNK15-AS1 increased in a dose-dependent manner, and the expression of HDAC1 and DNMT1 decreased in a dose-dependent manner (P<0.05; P<0.05; P<0.05; P<0.05). (B) The SCG7901 cells was treated with 5-azacytidine. The expression level of KCNK15-AS1 increased in a dose-dependent manner, and the expression of HDAC1 and DNMT1 decreased in a dose-dependent manner (P<0.05; P<0.05; P<0.05; P<0.05). (C) The BGC-823 cells were treated with chidamide. The expression level of KCNK15-AS1 increased in a dose-dependent manner, and the expression of HDAC1 and DNMT1 decreased in a dose-dependent manner (P<0.05; P<0.05; P<0.05; P<0.05). (D) The SCG7901 cells were treated with chidamide. The expression level of KCNK15-AS1 increased in a dose-dependent manner, and the expression of HDAC1 and DNMT1 decreased in a dose-dependent manner (P<0.05; P<0.05; P<0.05; P<0.05). (E) Western blot showed the expression levels of HDAC1 and DNMT1 in BGC-823 cells treated with chidamide and 5-azacytidine. (F) Western blot showed the expression levels of HDAC1 and DNMT1 in SCG7901 cells treated with chidamide and 5-azacytidine. (G) After treatment with chidamide and 5-azacytidine, KCNK15-AS1 was unmethylated in both the BGC-823 and SCG7901 cells. (H) The expression of KCNK15-AS1 was decreased after the knockdown of HDAC1 (P<0.05).