Fig. 6

SOX4 served as an oncogene and reversed the effects of METTL14 in CRC. a. The SOX4 knockdown efficiency was proved at the protein levels in HCT116 and HCT8 cells by western blot assay. b. Quantified results of the cell migration abilities of HCT116 and HCT8 cells with SOX4 deficiency. c. Quantified results of the cell invasion abilities of HCT116 and HCT8 cells with SOX4 deficiency. d. The protein levels of METTL14 and SOX4 in HCT116 and HCT8 cells transfected with METTL14 and SOX4 expression plasmid or blank vector (vector) were measured using western blot. e, f. Quantified results of the cell migration e and invasion f abilities of cell migration abilities of METTL14-overexpressing HCT116 and HCT8 cells added with SOX4 expression plasmid or blank vector. g. Left panel, representative images of the gross lesion in the lung tissues from sh-NC and shSOX4 group. Middle panel, quantification of the metastatic nodes from indicated groups. Right panel, representative microscopic views of pulmonary metastatic foci from indicated groups using HE staining. h. Left panel, representative images of the gross lesion in the lung tissues from negative control (NC), LV-METTL14 + vector and LV-METTL14 + SOX4 group. Middle panel, quantification of the metastatic nodes from indicated groups. Right panel, representative microscopic views of pulmonary metastatic foci from indicated groups using HE staining. **P < 0.01, ***P < 0.001