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Fig. 6 | Molecular Cancer

Fig. 6

From: M6A-mediated upregulation of circMDK promotes tumorigenesis and acts as a nanotherapeutic target in hepatocellular carcinoma

Fig. 6

ATG16L1 is responsible for circMDK-mediated proliferation, migration, invasion and apoptosis. A Cell proliferation assay for HCC cells with ATG16L1 overexpression and circMDK knockdown. *p < 0.05; **p < 0.01. B Representative images (left) and quantification (right) of the colony formation assay in HCC cells. *p < 0.05; **p < 0.01; ***p < 0.001. C Representative images (top) and quantification (bottom) of migration assays in HCC cells. **p < 0.01. D Representative images (top) and quantification (bottom) of invasion assays in HCC cells. **p < 0.01. E Representative images (left) and quantification (right) of apoptosis assays in HCC cells. **p < 0.01; ***p < 0.001. F Expression changes (left) and quantification (right) of ATG16L1, AKT, p-AKT, PI3K, p-PI3K, mTOR in Hep3B cells co-transfected with si-circMDK together with ATG16L1 overexpression or (G) si-ATG16L1 together with circMDK overexpression. *p < 0.05; **p < 0.01. H Schematic diagram of circMDK-miR-346/miR-874-3p-ATG16L1 axis. Data are shown as mean ± SD of three independent experiments

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