Skip to main content
Fig. 6 | Molecular Cancer

Fig. 6

From: m6A modification-mediated BATF2 acts as a tumor suppressor in gastric cancer through inhibition of ERK signaling

Fig. 6

METTL3-mediated m6A modification represses BATF2 expression in GC. a-b qRT-PCR and western blot assays showed the mRNA and protein expression, respectively, of BATF2 in GC cells with knockdown or overexpression of METTL3 (*P < 0.05; **P < 0.01). c m6A immunoprecipitation and qRT-PCR assays showed the relative percentage of BATF2 mRNA with methylation (*P < 0.05; **P < 0.01). d-e IHC staining of BATF2 and METTL3 in TMAs were presented, and their correlation was calculated. Scale bars = 200 μm. f Wild-type BATF2 3′UTR and BATF2 3′UTR with a mutation at the m6A consensus sequence were cloned into a luciferase reporter. Mutations of the m6A modification region were generated by replacing adenosine with thymine. g Relative luciferase activity of the wild-type and 3 mutant BATF2 3′UTR reporter vectors catalyzed by METTL3 (ns: no significant difference). h Proposed mechanism scheme of BATF2 in GC. The m6A modification of BATF2 mRNA by METTL3 represses its expression; BATF2 promotes the expression of p53 by suppressing its ubiquitination and degradation, which further decreased ERK signaling

Back to article page