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. 2022 Aug 28:2022:4522873.
doi: 10.1155/2022/4522873. eCollection 2022.

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

Wei Xu  1 , Laijian Zhang  1 , Zhi Chen  1 , Hao Wang  1 , Zhongyi Yan  1
Affiliations

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

Wei Xu et al. Emerg Med Int. .

Retraction in

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 > 0.05P>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.

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Conflict of interest statement

The authors declare that they have no conflicts of interest and the research was conducted in the absence of any commercial or financial relationships.

Figures

Figure 1
Figure 1
Impacts of PYM on protein expression of OC cells. (a) WB map. (b) PI3K/AKT/mTOR pathway protein expression. (c) Autophagy protein expression. Compared with the normal group, #P < 0.05. Compared with the L-PTM group, & P < 0.05.
Figure 2
Figure 2
Impacts of PYM on OC cell activity. (a) Cell growth curve. (b) Experimental results of colony formation assay. (c) Colony-forming efficiency. Compared with the normal group, #P < 0.05. Compared with the L-PTM group, & P < 0.05. Compared with the M-PTM group, ∗P < 0.05.
Figure 3
Figure 3
Impacts of PYM on OC cell apoptosis rate. (a) FCM results. (b) Apoptosis rate. Compared with the normal group, #P < 0.05; compared with the L-PTM group, & P < 0.05.
Figure 4
Figure 4
PYM influences OC autophagy via PI3K/AKT/mTOR axis. (a) WB map. (b) PI3K/AKT/mTOR pathway protein expression. (c) Autophagy protein expression. Compared with the normal group, #P < 0.05; compared with the PYM + 740Y-P group, & P < 0.05.
Figure 5
Figure 5
PYM influences OC cell apoptosis via PI3K/AKT/mTOR axis. (a) Cell growth curve. (b) Experimental results of colony formation assay. (c) Colony-forming efficiency. Compared with the normal group, #P < 0.05; compared with the PYM + 740Y-P group, & P < 0.05.
Figure 6
Figure 6
PYM influences OC cell activity via the PI3K/AKT/mTOR axis. (a) FCM results. (b) Apoptosis rate. Compared with the normal group, #P < 0.05; compared with the PYM + 740Y-P group, & P < 0.05.
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