Research Paper Volume 12, Issue 24 pp 24967—24982

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

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.