Fig. 6

High MKRN1 levels promote the TGF-β signalling via SNIP1 ubiquitination and degradation. A, B WB was used to detect the effect of SNIP1 on the TGF-β pathway. CTGF-β1 expression was shown to be inversely associated to the prognosis of CRC patients. D Spearman correlation analysis between MKRN1 and the TGF-β pathway. E, F WB detection of TGF-β pathway-related factors after MKRN1 knockdown and overexpression. G TGF-β1 treatment reversed the inhibition of EMT and TGF-β signalling-related molecules induced by MKRN1 knockdown. H LY2109761 treatment reversed the activation of EMT and TGF-β signalling-related molecules induced by MKRN1 overexpression. I TGF-β1 treatment reversed the impaired migratory capacity of HCT116 cells caused by MKRN1 knockdown (Scale bar: 50 µm). J LY2109761 treatment reversed the increased migratory capacity of HCT15 cells caused by MKRN1 overexpression (Scale bar: 50 µm). K Expression of major TGF-β signalling markers after co-transfection of HCT116 cells with Control, sh1-MKRN1, and sh-SNIP1. L Expression of major TGF-β signalling markers after HCT15 cell co-transfection with vector, OE-MKRN1, and OE-SNIP1. M Representative graphs of MKRN1, SNIP1, and TGF-β1 expression in CRC detected by immunohistochemistry (scale bar: 100 µm; scale bar: 50 µm). ** P < 0.01, *** P < 0.001