Fig. 4

MDM2 is a major contributor to the function of NAT10 in gastric carcinogenesis. A Overexpression of MDM2 inhibited the upregulation of p53 and p21 proteins in NAT10-knockout AGS cells, while knockdown of MDM2 effectively reversed the inhibitory effect of NAT10 overexpression on p53 and p21. B MDM2 overexpression reversed the upregulation of p53 and p21 proteins by NAT10 knockdown in BGC823 cells. C and D The effects of NAT10 depletion on cell proliferation (C) and colonic growth (D) were rescued by transfection with MDM2, whereas cell proliferation and colonic growth of NAT10-overexpressing cells were prevented by knockdown of MDM2. E and F Cell cycle (E) and apoptosis (F) were measured in the indicated cells by flow cytometry. G MDM2 and NAT10 proteins were evaluated in NAT10-knockout AGS cells stably expressing MDM2 or vector control. H MDM2 overexpression rescued the impaired capacity of tumor growth triggered by NAT10 knockout (n = 5 mice/group). Error bars, SD. *P < 0.05, **P < 0.01, ***P < 0.001 using a two-tailed t-test