Pingyangmycin Activates Oral Carcinoma Cell Autophagy via the Phosphorylation of the PI3K/AKT/mTOR Axis to Achieve the Purpose of Treating Oral Carcinoma

Abstract

Objective. The aim of the study is to investigate the role of pingyangmycin (PYM) in oral carcinoma (OC) cell autophagy via the PI3K/AKT/mTOR axis. Methods. 200 μL PYM culture solution with a concentration of 100 μg/ml (low PYM (L-PYM) group), 300 μg/ml (middle PYM (M-PYM) group), 500 μg/ml (high PYM (H-PYM) group), and the same amount of conventional medium (normal control (NC)) were added to the purchased OC cell line SCC-25, respectively, and the PI3K/AKT/mTOR pathway expression, autophagy protein levels, cell activity, and apoptosis rate were determined. Subsequently, we selected OC cells co-cultured with PYM with the concentration of the most significant intervention effect and 740Y-P, a specific activator of the PI3K/AKT/mTOR axis, and those treated with 740Y-P alone for the aforementioned detection. Results. L-PYM, M-PYM, and H-PYM groups all showed decreased PI3K, AKT, mTOR, and phosphorylated protein levels ( $P<0.05$ ). Beclin1 and LC3-II protein levels and apoptosis rate of PYM-intervened OC cells increased, but the activity decreased ( $P<0.05$ ). Under 740Y-P intervention, the PI3K/AKT/mTOR pathway was activated, cell activity was increased, and the apoptosis rate and autophagy were decreased ( $P<0.05$ ). Simultaneous use of PYM and 740Y-P led to no difference in cell condition compared with NC ( $P>0.05$ P>0.05). Conclusion. PYM can activate OC cell autophagy by inhibiting the phosphorylation of the PI3K/AKT/mTOR axis, and thus, achieving the goal of killing tumor cells.