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Paclitaxel is not as effective for neuroblastoma as most of the front‐line chemotherapeutics due to drug resistance. This study explored the regulatory mechanism of paclitaxel‐associated autophagy and potential solutions to paclitaxel resistance in neuroblastoma. The formation of autophagic vesicles was detected by scanning transmission electron microscopy and flow cytometry. The autophagy‐associated proteins were assessed by western blot. Autophagy was induced and the autophagy‐associated proteins  LC 3‐I,  LC 3‐ II , Beclin 1, and thioredoxin‐related protein 14 ( TRP 14), were found to be upregulated in neuroblastoma cells that were exposed to paclitaxel. The inhibition of Beclin 1 or  TRP 14 by si RNA  increased the sensitivity of the tumor cells to paclitaxel. In addition, Beclin 1‐mediated autophagy was regulated by  TRP 14. Furthermore, the  TRP 14 inhibitor suberoylanilide hydroxamic acid ( SAHA ) downregulated paclitaxel‐induced autophagy and enhanced the anticancer effects of paclitaxel in normal control cancer cells but not in cells with upregulated Beclin 1 and  TRP 14 expression. Our findings showed that paclitaxel‐induced autophagy in neuroblastoma cells was regulated by  TRP 14 and that  SAHA  could sensitize neuroblastoma cells to paclitaxel by specifically inhibiting  TRP 14.

Suberoylanilide hydroxamic acid sensitizes neuroblastoma to paclitaxel by inhibiting thioredoxin‐related protein 14‐mediated autophagy