Research Paper Volume 12, Issue 24 pp 24967—24982

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

Figure 2. Silencing HBXIP inhibits GC cell viability, migration and invasion, and induces apoptosis. (A) Representative Western blots of HBXIP protein and its quantitation in AGS and MKN-45 cells upon HBXIP silencing, normalized to GAPDH. (B) CCK-8 was used to examine the proliferation of AGS and MKN-45 cells upon HBXIP silencing. (C) Transwell assay was used to examine the migration and invasion ability of AGS and MKN-45 cells upon HBXIP silencing (× 200). (D) Flow cytometry was used to examine the apoptosis of AGS and MKN-45 cells upon HBXIP silencing. * p < 0.05 vs. the sh-NC group (AGS or MKN-45 cells treated with sh-NC). The above data were measurement data, and expressed as mean ± standard deviation. Data in panels (A, C and D) were analyzed by one-way ANOVA with Tukey’s post hoc test and in panel B by repeated measures ANOVA with Bonferroni post hoc test. The cell experiment was repeated 3 times independently.