Fig. 5.

miR-22/KAT6B determines cellular fate via Akt-NF-kB pathway. a and b miR-22 overexpression or KAT6B knockdown inhibited PI3K/Akt/NF-κB activity in CAL27 cells. In contrast, miR-22 inhibition further promoted PI3K/Akt/NF-κB activity (c). d-e, The inhibition rate was calculated 72 h later after the initial treatment of CAL27 cells. The data were obtained from three independent experiments in triplicate versus no treatment or control treatment; (f-g) qRT-PCR showed that miR-22 overexpression or KAT6B knockdown reduced S100A8, PDGF and VEGF expression. h, mixed cytokines S100A8, PDGF and VEGF attenuated inhibition of NF-kB activity in miR-22-overexpressing or shKAT6b tongue cancer cells. The data shown here are the mean ± SD from three independent experiments conducted in triplicate, versus control *p < 0.05. i, Ectopic xenograft tissue obtained from the previous animal experiment, which were fixed by formaldehyde, paraffin embedded, continuous sliced and tested for the immunization of KAT6B and AKT signaling molecules. The representative images are shown