Related Experiment Video

Updated: Jan 23, 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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RIPK2 induces docetaxel resistance in prostate cancer through the NF-κB/P-gp signaling pathway

Shaoqiang Xing1,2, Zhaoliang Xu1,2, Sheng Zeng2

  • 1The First Central Clinical School, Tianjin Medical University, Tianjin, China.

Plos One
|January 21, 2026
PubMed

Insights

Receptor-interacting protein kinase 2 (RIPK2) drives docetaxel resistance in prostate cancer by activating the NF-κB/P-glycoprotein pathway. Inhibiting RIPK2 may overcome chemoresistance in prostate cancer patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Chemoresistance is a major challenge in prostate cancer treatment.
  • The role of Receptor-interacting protein kinase 2 (RIPK2) in prostate cancer chemoresistance is not well understood.

Purpose of the Study:

  • To investigate the role and mechanism of RIPK2 in docetaxel (DTX) resistance in prostate cancer.
  • To analyze RIPK2 expression in prostate cancer tissues and cell lines.

Main Methods:

  • Analysis of The Cancer Genome Atlas (TCGA) data for RIPK2 expression.
  • In vitro studies using docetaxel-resistant prostate cancer cell lines.
  • Mechanistic investigations involving signaling pathways and protein expression.
  • In vivo xenograft tumor experiments.

Main Results:

  • RIPK2 expression was elevated in prostate cancer tissues and associated with poor pathological grading.
  • RIPK2 was upregulated in multiple docetaxel-resistant prostate cancer cell lines.
  • RIPK2 mediated docetaxel resistance by upregulating P-glycoprotein (P-gp) via NF-κB pathway activation.
  • Inhibition of RIPK2 or P-gp enhanced docetaxel efficacy in vivo.

Conclusions:

  • RIPK2 plays a critical role in mediating docetaxel resistance in prostate cancer.
  • The NF-κB/P-gp signaling pathway is a key mechanism by which RIPK2 confers chemoresistance.
  • RIPK2 and its downstream targets represent potential therapeutic targets for overcoming chemoresistant prostate cancer.

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