Paclitaxel promotes mTOR signaling‐mediated apoptosis in esophageal cancer cells by targeting MUC20

Abstract

Abstract 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.

Keywords

• drug target
• esophageal cancer
• mTOR signaling
• MUC20
• paclitaxel