Related Experiment Video

Updated: Feb 14, 2026

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel
06:44

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel

Published on: September 8, 2017

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

Quan Wang1,2, Wei-Yang He1, Yi-Zhou Zeng1,2

  • 1Department of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.

International Urology and Nephrology
|February 21, 2018
PubMed
Abstract

Insights

Tea polyphenols (TP) inhibit protective autophagy induced by docetaxel in castration-resistant prostate cancer (CRPC) cells. This combination therapy enhances apoptosis and improves treatment outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Investigates docetaxel resistance mechanisms in human castration-resistant prostate cancer (CRPC) cell lines (PC3 and DU145).
  • Examines the role of tea polyphenols (TP) in modulating autophagy in CRPC.

Purpose of the Study:

  • To elucidate the mechanism of docetaxel resistance in CRPC.
  • To explore the therapeutic potential of combining tea polyphenols with docetaxel.
  • To understand the impact of TP on autophagy pathways in CRPC cells.

Main Methods:

  • Immunofluorescence assays and flow cytometry (Annexin V-FITC/PI) to assess apoptosis and autophagy.
  • Western blot analysis to detect autophagy-related protein expression.
  • Utilized human CRPC cell lines (PC3 and DU145).

Main Results:

  • Docetaxel induced autophagy and apoptosis, increasing p-JNK, p-Bcl-2, and Beclin1 expression.
  • Co-administration of TP with docetaxel decreased autophagy but increased apoptosis.
  • TP combination therapy upregulated p-mTOR expression in CRPC cells.

Conclusions:

  • Docetaxel triggers protective autophagy via JNK pathway activation, Bcl-2 phosphorylation, and Beclin1 dissociation in CRPC.
  • Tea polyphenols activate the mTOR pathway, suppressing docetaxel-induced autophagy.
  • Combining TP with docetaxel enhances therapeutic efficacy in CRPC cells by overcoming protective autophagy.
Keywords:
AutophagyCastration-resistant prostate cancerDocetaxel resistanceTea polyphenol

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