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Updated: Jul 15, 2025

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Published on: May 14, 2016
Paclitaxel promotes mTOR signaling-mediated apoptosis in esophageal cancer cells by targeting MUC20
Meng Li1,2, Zhen Feng1,2, Rui Han3
1Department of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Background:
The aim of this study was to analyze the effect of paclitaxel on the apoptosis of esophageal cancer cells in relation to MUC20.
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.
Insights
Paclitaxel induces apoptosis in esophageal cancer cells by upregulating MUC20, which activates mTOR signaling. This pathway, involving PKM2, offers a therapeutic target for esophageal cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Esophageal cancer remains a significant health concern.
- Understanding the molecular mechanisms of chemotherapy resistance is crucial.
- Mucins, like MUC20, play diverse roles in cancer progression.
Purpose of the Study:
- To investigate the role of MUC20 in paclitaxel-induced apoptosis of esophageal cancer cells.
- To elucidate the signaling pathways involved in this process.
- To evaluate MUC20 as a potential therapeutic target.
Main Methods:
- Quantitative real-time PCR (RT-qPCR)
- Cell Counting Kit-8 (CCK-8) assay
- Western blotting
- Flow cytometry
- In vivo studies using a nude mouse model
Main Results:
- Paclitaxel treatment significantly upregulated MUC20 expression in esophageal cancer cells.
- Both paclitaxel and MUC20 overexpression reduced cell viability and enhanced apoptosis.
- mTOR signaling pathway activation and downstream PKM2 upregulation were observed.
- Inhibition of mTOR signaling attenuated paclitaxel's effects.
- Tumor growth was suppressed in vivo with MUC20 overexpression.
Conclusions:
- MUC20 is a key mediator of paclitaxel's anti-cancer effects in esophageal cancer.
- Paclitaxel promotes apoptosis via MUC20-mediated activation of the mTOR signaling pathway.
- Targeting MUC20 and the mTOR pathway presents a promising therapeutic strategy.
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