METTL5 promotes gastric cancer progression via sphingomyelin metabolism

Figure 3 METTL5 knockdown inhibited the malignant phenotype of gastric cancer cells. A: Western blot of METTL5 knockdown efficiency in HGC-27 and AGS cells; B and C: Reverse-transcription PCR of the knockout efficiency of METTL5 in HGC-27 and AGS cells; D and E: RNA expression of TRMT112 in HGC-27 and AGS after METTL5 knockdown; F and G: The Cell Counting Kit-8 assay experiment assay to detect the proliferation ability of HGC-27 and AGS cells after METTL5 knockdown; H and I: Clone formation assay to detect the proliferation ability of HGC-27 and AGS cells after METTL5 knockdown; J and K: Transwell assay to detect invasion ability of HGC-27 and AGS cells after METTL5 knockdown; L and M: A wound-healing motility assay was used to detect the migration ability of HGC-27 and AGS cells after METTL5 knockdown; N and O: Flow cytometry was used to detect the apoptosis of HGC-27 and AGS cells after METTL5 knockdown. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001.