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. 2021 Apr 2;12(11):3209–3221. doi: 10.7150/jca.50403

Figure 6.

Figure 6

METTL3 was a direct target of miR-193b-5p and positively regulated by BLACAT2. A: The predicted potential binding sites of miR-193b-5p with the 3′‐UTR of METTL3. The mutated version of the METTL3 3′‐UTR was also given. B: Luciferase reporter assay showed that miR‐193b-5p mimic suppressed the activity of METTL3 3′‐UTR‐wt reporter in AGS cells. C: MiR-193b-5p overexpression significantly inhibited the expression of METTL3 in gastric cancer cells at mRNA levels through qRT‐PCR. D-E: Expression intensity of METTL3 was analyzed in gastric cancer tissues and normal control tissues according to the oncomine dataset. F-G: CCK8 and plate colony formation experiments demonstrated that METTL3 knockdown partly abolished the promotion effects of the proliferation of AGS and MGC-803 cells transfected with miR‐193b-5p inhibitor. H: Flow cytometry experiment proved that METTL3 knockdown partly weakened the inhibitory effects of apoptosis of AGS and MGC-803 cells transfected with miR‐193b-5p inhibitor. I: METTL3 expression was repressed by miR-193b-5p mimics in AGS and MGC803 cells at the protein level by western-blot analysis. J: Relative expression of METTL3 was suppressed by BLACAT2 silencing confirmed by western-blot analysis. Data was presented as means ± SD (*p < 0.05, **p < 0.01, and ***p < 0.001, Ns : Statistically no sense).