Research Paper Volume 12, Issue 24 pp 24967—24982

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

Figure 5. METTL3 inhibits GC cell viability, migration and invasion, and induces apoptosis by mediating MYC mRNA m6A modification. (A) Representative Western blots of MYC protein and its quantitation in GC cells treated with oe-MYC or combined with sh-METTL3-1, normalized to GAPDH. (B) Me-RIP and RT-qPCR were used to examine m6A levels of MYC mRAN in GC cells treated with oe-MYC or combined with sh-METTL3-1. (C) The binding of METTL3 to MYC mRNA assessed by PAR-CLIP assay in GC cells treated with oe-MYC or combined with sh-METTL3-1. (D) CCK-8 was used to examine the proliferation of GC cells treated with oe-MYC or combined with sh-METTL3-1. (E) Transwell was used to examine the migration and invasion of GC cells treated with oe-MYC or combined with sh-METTL3-1 (× 200). (F) Flow cytometry was used to examine the apoptosis of GC cells treated with oe-MYC or combined with sh-METTL3-1. * p < 0.05 vs. the oe-NC group (GC cells treated with oe-NC). # p < 0.05 vs. the sh-NC + oe-MYC group (GC cells treated with sh-NC and oe-MYC). The above data were all measured data, expressed as mean ± standard deviation. Data in panels (AC, E and F) by one-way ANOVA with Tukey’s post hoc test, and in panel D by repeated measures ANOVA with Bonferroni post hoc test. The cell experiment was repeated 3 times independently.