Figure 4.

Per1 inhibits autophagy in oral squamous cell carcinoma (OSCC) cells and the apoptosis and proliferation of OSCC cells by regulating the AKT/mTOR pathway. A, Transmission electron microscopy experiments revealed that after addition of the AKT activator SC79 to Per1‐OE SCC15 cells, the autophagosome density was significantly reduced (low magnification scale bars = 2 μm; high magnification scale bars = 1 μm). B, Flow cytometry showed that the apoptotic index of Per1‐OE SCC15 cells was significantly reduced after addition of the AKT activator SC79. C, TUNEL assay indicated that the increased TUNEL‐positive rate in Per1‐OE SCC15 cells was remarkably rescued after addition of the AKT activator SC79. D, Western blotting showed that the decreased protein expression of p‐AKT, p‐mTOR and P62 in Per1‐OE SCC15 cells was remarkably increased after addition of the AKT activator SC79, while the increased protein expression of Beclin1 and LC3BII/LC3BIratio were remarkably decreased. E, CCK8 and MTT assays revealed that the proliferation of Per1‐OE SCC15 cells was significantly increased after addition of the AKT activator SC79. F, Western blotting showed that the increased expression of LC3BII in Per1‐OE SCC15 cells with CQ was remarkably decreased after addition of the AKT activator SC79, while the expression of P62 was remarkably increased. All data represent three independent experiments. The results are shown as the mean ± SD (n ≥ 3). *P < .05; **P < .01; ***P < .001; ****P < .0001