Research Paper Volume 12, Issue 24 pp 24967—24982

HBXIP promotes gastric cancer via METTL3-mediated MYC mRNA m6A modification

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Figure 3. Silencing HBXIP diminishes the expression pattern of METTL3 and inhibits GC cell viability, migration and invasion, and induces apoptosis. (L) Viability of AGS and MKN-45 cells examined by CCK-8 assay upon HBXIP silencing or combined with METTL3 overexpression. (M) Migration and invasion of AGS and MKN-45 cells were examined by Transwell assay upon HBXIP silencing or combined with METTL3 overexpression (× 200). (N) Apoptosis of AGS and MKN-45 cells examined by flow cytometry upon HBXIP silencing or combined with METTL3 overexpression. * p < 0.05 vs. the sh-NC or sh-NC and oe-NC group (AGS or MKN-45 cells treated with sh-NC or both sh-NC and oe-NC). # p < 0.05 vs. the sh-HBXIP and oe-NC group (AGS or MKN-45 cells treated with both sh-HBXIP and oe-NC). The above results were measurement data, and expressed as mean ± standard deviation. Data in panels B and C were compared by paired t test, in panels (DG, IK, M and N) were analyzed by one-way ANOVA with Tukey’s post hoc test, and in panels H and L by repeated measures ANOVA with Bonferroni post hoc test. The cell experiment was repeated 3 times independently.