Fig. 1.

EMT in cancer cells is regulated by m⁶A levels of mRNAs. a HeLa and HepG2 cells were treated with or without 10 ng/ml TGF-β for 3 days, the m⁶A/A ratio of the total mRNA were determined by LC–MS/MS. b Wound healing of wild-type (control) or Mettl3 ^Mut/− cells was recorded (left) and quantitatively analyzed (right). c Wild-type or Mettl3 ^Mut/− cells were allowed to invade for 24 h and tested by CytoSelect™ 24-well Cell Invasion assay kits (8 µm, colorimetric format); d, e mRNA (d) and protein (e) expressions of MMP2, FN, and E-Cad in wild-type and Mettl3 ^Mut/− HeLa cells were measured by qRT-PCR and western blot analysis, respectively. f HeLa cells were transfected with pcDNA/ALKBH5 or a vector control for 48 h, protein expression was determined by western blot analysis (left) and quantitatively analyzed (right). g Wild-type or Mettl3 ^Mut/− cells were treated with or without 10 ng/ml TGF-β for 3 days, protein expression was determined by western blot analysis (left) and quantitatively analyzed (right). h The expression of METTL3 in liver cancer and its matched adjacent normal tissues of 50 patients from TCGA database. i Correlation between METTL3 and CDH1 in liver cancer patients (n = 364) from TCGA database. j HeLa cells were pretreated with or without Smad2/3 inhibitor SB431542 (10 μM) and then further treated with 10 ng/ml TGF-β for 3 days, the m⁶A/A ratio of the total mRNA were determined by LC–MS/MS. Data are presented as means ± SD from three independent experiments. *p < 0.05, **p < 0.01, NS, no significant, by Student’s t test. Red bar = 200 μm