Pingyangmycin Activates Oral Carcinoma Cell Autophagy via the Phosphorylation of the PI3K/AKT/mTOR Axis to Achieve the Purpose of Treating Oral Carcinoma
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 PY...
Saved in:
| Main Authors: | , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2022-01-01
|
| Series: | Emergency Medicine International |
| Online Access: | http://dx.doi.org/10.1155/2022/4522873 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1850210578298044416 |
|---|---|
| author | Wei Xu Laijian Zhang Zhi Chen Hao Wang Zhongyi Yan |
| author_facet | Wei Xu Laijian Zhang Zhi Chen Hao Wang Zhongyi Yan |
| author_sort | Wei Xu |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-927412027489405dab089b4eef65b89a |
| institution | OA Journals |
| issn | 2090-2859 |
| language | English |
| publishDate | 2022-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Emergency Medicine International |
| spelling | doaj-art-927412027489405dab089b4eef65b89a2025-08-20T02:09:45ZengWileyEmergency Medicine International2090-28592022-01-01202210.1155/2022/4522873Pingyangmycin Activates Oral Carcinoma Cell Autophagy via the Phosphorylation of the PI3K/AKT/mTOR Axis to Achieve the Purpose of Treating Oral CarcinomaWei Xu0Laijian Zhang1Zhi Chen2Hao Wang3Zhongyi Yan4Department of Oral and Maxillofacial SurgeryDepartment of Oral and Maxillofacial SurgeryDepartment of Oral and Maxillofacial SurgeryDepartment of Oral and Maxillofacial SurgeryDepartment of Oral and Maxillofacial SurgeryObjective. 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.http://dx.doi.org/10.1155/2022/4522873 |
| spellingShingle | Wei Xu Laijian Zhang Zhi Chen Hao Wang Zhongyi Yan Pingyangmycin Activates Oral Carcinoma Cell Autophagy via the Phosphorylation of the PI3K/AKT/mTOR Axis to Achieve the Purpose of Treating Oral Carcinoma Emergency Medicine International |
| title | Pingyangmycin Activates Oral Carcinoma Cell Autophagy via the Phosphorylation of the PI3K/AKT/mTOR Axis to Achieve the Purpose of Treating Oral Carcinoma |
| title_full | Pingyangmycin Activates Oral Carcinoma Cell Autophagy via the Phosphorylation of the PI3K/AKT/mTOR Axis to Achieve the Purpose of Treating Oral Carcinoma |
| title_fullStr | Pingyangmycin Activates Oral Carcinoma Cell Autophagy via the Phosphorylation of the PI3K/AKT/mTOR Axis to Achieve the Purpose of Treating Oral Carcinoma |
| title_full_unstemmed | Pingyangmycin Activates Oral Carcinoma Cell Autophagy via the Phosphorylation of the PI3K/AKT/mTOR Axis to Achieve the Purpose of Treating Oral Carcinoma |
| title_short | Pingyangmycin Activates Oral Carcinoma Cell Autophagy via the Phosphorylation of the PI3K/AKT/mTOR Axis to Achieve the Purpose of Treating Oral Carcinoma |
| title_sort | pingyangmycin activates oral carcinoma cell autophagy via the phosphorylation of the pi3k akt mtor axis to achieve the purpose of treating oral carcinoma |
| url | http://dx.doi.org/10.1155/2022/4522873 |
| work_keys_str_mv | AT weixu pingyangmycinactivatesoralcarcinomacellautophagyviathephosphorylationofthepi3kaktmtoraxistoachievethepurposeoftreatingoralcarcinoma AT laijianzhang pingyangmycinactivatesoralcarcinomacellautophagyviathephosphorylationofthepi3kaktmtoraxistoachievethepurposeoftreatingoralcarcinoma AT zhichen pingyangmycinactivatesoralcarcinomacellautophagyviathephosphorylationofthepi3kaktmtoraxistoachievethepurposeoftreatingoralcarcinoma AT haowang pingyangmycinactivatesoralcarcinomacellautophagyviathephosphorylationofthepi3kaktmtoraxistoachievethepurposeoftreatingoralcarcinoma AT zhongyiyan pingyangmycinactivatesoralcarcinomacellautophagyviathephosphorylationofthepi3kaktmtoraxistoachievethepurposeoftreatingoralcarcinoma |