Inhibiting autophagy overcomes docetaxel resistance in castration-resistant prostate cancer cells.

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  • Additional Information
    • Source:
      Publisher: Springer Country of Publication: Netherlands NLM ID: 0262521 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1573-2584 (Electronic) Linking ISSN: 03011623 NLM ISO Abbreviation: Int Urol Nephrol Subsets: MEDLINE
    • Publication Information:
      Publication: Amsterdam : Springer
      Original Publication: Budapest, Akademiai KiadoĢ
    • Subject Terms:
      Drug Resistance, Neoplasm*; Antineoplastic Agents/*pharmacology ; Autophagy/*drug effects ; Polyphenols/*pharmacology ; Prostatic Neoplasms, Castration-Resistant/*drug therapy ; Taxoids/*pharmacology; Antineoplastic Agents/therapeutic use ; Apoptosis/drug effects ; Beclin-1/metabolism ; Cell Line, Tumor ; Docetaxel ; Humans ; JNK Mitogen-Activated Protein Kinases/metabolism ; MAP Kinase Signaling System/drug effects ; Male ; Phosphorylation ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Taxoids/therapeutic use ; Tea
    • Abstract:
      Background: This study investigates the docetaxel-resistant mechanism and explores the effect of tea polyphenols (TP) on autophagy and its related mechanism in human castration-resistant prostate cancer (CRPC) cell lines PC3 and DU145.
      Methods: Immunofluorescence assay and annexin V-FITC/PI double staining flow cytometry were used to analyze the apoptosis and autophagy of PC3 and DU145 cells. The expression of autophagy-related proteins was detected by western bolt.
      Results: Docetaxel could induce autophagy and apoptosis, together with the expression increase in p-JNK, p-Bcl-2 and Beclin1. The level of autophagy was remarkably decreased, but apoptosis was increased after combining with TP. In addition, the expression of p-mTOR was increased after combining with TP.
      Conclusion: Docetaxel induces protective autophagy in CRPC cells by JNK pathway activation and then Bcl-2 phosphorylation and Beclin1 dissociation. TP activates mTOR pathway, which ultimately inhibits docetaxel-induced autophagy and improves therapeutic efficacy of docetaxel in CRPC cells.
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    • Grant Information:
      81372758 the Natural Science Foundation of China; cstc2013jcycA10058 the Natural Science Found Project of Chongqing; 2013-1-006 the Municipal Health Bureau of Chongqing
    • Contributed Indexing:
      Keywords: Autophagy; Castration-resistant prostate cancer; Docetaxel resistance; Tea polyphenol
    • Accession Number:
      0 (Antineoplastic Agents)
      0 (BECN1 protein, human)
      0 (Beclin-1)
      0 (Polyphenols)
      0 (Proto-Oncogene Proteins c-bcl-2)
      0 (Taxoids)
      0 (Tea)
      15H5577CQD (Docetaxel)
      EC 2.7.1.1 (MTOR protein, human)
      EC 2.7.11.1 (TOR Serine-Threonine Kinases)
      EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
    • Publication Date:
      Date Created: 20180221 Date Completed: 20180927 Latest Revision: 20211204
    • Publication Date:
      20231215
    • Accession Number:
      PMC5878207
    • Accession Number:
      10.1007/s11255-018-1801-5
    • Accession Number:
      29460131