Fig. 4: p53 phosphorylation mediates SIRT4-induced autophagy in PDAC.

A Representative images (left) and its quantification (right panel) of the autophagic flux detection with the mRFP-GFP-LC3 reporter in Capan-2 cells co-transfected with control, SIRT4, or SIRT4H161Y vectors, respectively, in the absence or presence of pifithrin-α, the inhibitor of p53 signaling pathway. B Representative images (left) and its quantification (right panel) of the autophagic flux detection with the mRFP-GFP-LC3 reporter in CCC-HPE-2 cells co-transfected with scramble or sh-SIRT4 vectors, respectively, in the absence or presence of Inauhzin, the activator of p53 signaling pathway. C In PDAC cell lines overexpressing SIRT4, the expression of p53 was transiently depleted, and LC3-GFP puncta in cells were observed. D After p53 signaling pathway inhibitors were used to treat PDAC cells overexpressing SIRT4 and its control cell line, the expressions of ARGs were detected by western blotting analysis. E SIRT4-depleted PDAC cell lines and control cell lines were treated with a p53 signaling pathway activator, the expressions of ARGs were detected by western blotting analysis. F Soft Agar technology was used to observe the effect of the p53 signaling pathway on the function of SIRT4. G SEM was applied for the detection of autophagy in tumor tissues of nude mice subcutaneously injected with Capan-2 and CCC-HPE-2 cells mentioned above. H Western blotting analysis was used to detect the expressions of ARGs in tumor tissues of nude mice subcutaneously injected with Capan-2 and CCC-HPE-2 cells mentioned above. GraphPad software was used for independence Sample t-test, (*P < 0.05; **P < 0.01; ***P < 0.001).