Abstract | BACKGROUND: METHODS: RT-qPCR analysis, a CCK-8 assay, western blotting, and flow cytometry were used to analyze the anticancer effects of paclitaxel treatment or OE-MUC20 in vitro and in vivo. RESULTS: The in vitro results showed that paclitaxel significantly induced MUC20 upregulation and that paclitaxel treatment or OE-MUC20 significantly decreased esophageal cancer cell viability and increased mTOR signaling activation and apoptosis. In addition, PKM2, a key downstream molecule of mTOR signaling, similarly showed significant upregulation after paclitaxel treatment in cells with OE-MUC20, and its expression was attenuated after treatment with mTOR inhibitors. In a nude mouse model, tumor growth was slow in the OE-MUC20 group and accelerated after inhibition of mTOR signaling. CONCLUSION: These data suggest that MUC20 is an important target of paclitaxel in esophageal cancer and promotes apoptosis through activation of mTOR signaling.
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Authors | Meng Li, Zhen Feng, Rui Han, Benchuang Hu, Renfeng Zhang, Hui Wang |
Journal | Thoracic cancer
(Thorac Cancer)
Vol. 14
Issue 31
Pg. 3089-3096
(11 2023)
ISSN: 1759-7714 [Electronic] Singapore |
PMID | 37772424
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2023 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd. |
Chemical References |
- Paclitaxel
- TOR Serine-Threonine Kinases
- MUC20 protein, human
- Mucins
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Topics |
- Humans
- Animals
- Mice
- Esophageal Neoplasms
(drug therapy, genetics)
- Apoptosis
- Cell Survival
- Mice, Nude
- Paclitaxel
(pharmacology)
- TOR Serine-Threonine Kinases
- Cell Line, Tumor
- Cell Proliferation
- Mucins
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