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 (). Beclin1 and LC3-II protein levels and apoptosis rate of PYM-intervened OC cells increased, but the activity decreased (). Under 740Y-P intervention, the PI3K/AKT/mTOR pathway was activated, cell activity was increased, and the apoptosis rate and autophagy were decreased (). Simultaneous use of PYM and 740Y-P led to no difference in cell condition compared with NC (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.

中文翻译：

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平阳霉素通过PI3K/AKT/mTOR轴磷酸化激活口腔癌细胞自噬达到治疗口腔癌的目的


客观的。本研究的目的是探讨平阳霉素 (PYM) 通过 PI3K/AKT/mTOR 轴在口腔癌 (OC) 细胞自噬中的作用。方法。 200 μL PYM培养液，浓度为100 μg /ml（低PYM（L-PYM）组）、300 μg /ml（中PYM（M-PYM）组）、500 μg /ml（高PYM组） (H-PYM组)和等量常规培养基(正常对照(NC))分别加入购买的OC细胞系SCC-25中，检测PI3K/AKT/mTOR通路表达量、自噬蛋白水平、测定细胞活性和凋亡率。随后，我们选择与干预效果最显着浓度的PYM和PI3K/AKT/mTOR轴特异性激活剂740Y-P共培养的OC细胞，以及单独用740Y-P处理的OC细胞进行上述检测。结果。 L-PYM、M-PYM 和 H-PYM 组均表现出 PI3K、AKT、mTOR 和磷酸化蛋白水平降低（ ）。 PYM干预的OC细胞中Beclin1和LC3-II蛋白水平和凋亡率增加，但活性降低（ ）。 740Y-P干预下，PI3K/AKT/mTOR通路被激活，细胞活性增加，细胞凋亡率和自噬降低（ ）。同时使用 PYM 和 740Y-P 与 NC 相比，细胞状况没有差异（ P>0.05）。结论。 PYM可以通过抑制PI3K/AKT/mTOR轴的磷酸化来激活OC细胞自噬，从而达到杀伤肿瘤细胞的目的。