Research Paper Volume 12, Issue 24 pp 24967—24982

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

Figure 6. Silencing HBXIP impairs METTL3-mediated MYC m6A mRNA modification in vitro. (A) Representative Western blots of HBXIP, METTL3 and MYC proteins and their quantitation in AGS and MKN-45 cells treated with sh-HBXIP, oe-METTL3 or both, normalized to GAPDH. (B) m6A levels of MYC mRNA were examined by Me-RIP and RT-qPCR in AGS and MKN-45 cells treated with sh-HBXIP, oe-METTL3 or both. (C) The binding of METTL3 to MYC mRNA assessed by PAR-CLIP assay in GC cells treated with sh-HBXIP, oe-METTL3 or both. * p < 0.05 vs. the sh-NC and oe-METTL3 group (AGS or MKN-45 cells treated with sh-NC and oe-NC, # p < 0.05 vs. the sh-HBXIP + oe-NC group (AGS or MKN-45 cells treated with sh-HBXIP and oe-NC), & p < 0.05 vs. the sh-NC + oe-METTL3 group (AGS or MKN-45 cells treated with sh-NC and oe-METTL3). The above results were measurement data, and expressed as mean ± standard deviation, and compared using one-way ANOVA with Tukey’s post hoc test. The cell experiment was repeated 3 times independently.