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January 24, 2026Open Access

RIPK2 induces docetaxel resistance in prostate cancer through the NF-κB/P-gp signaling pathway.

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Authors

SXShaoqiang XingZXZhaoliang XuSZSheng Zeng

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Overview

Analysis of RIPK2's role reveals it induces docetaxel resistance in prostate cancer, suggesting new treatment targets.

Key Points

  • This research aims to clarify the role of RIPK2 in chemoresistance in prostate cancer, particularly to docetaxel.
  • Analyzed RIPK2 expression data from The Cancer Genome Atlas.
  • Investigated association of RIPK2 with clinicopathological features.
  • Conducted mechanistic experiments to assess RIPK2's role in docetaxel resistance.
  • Performed xenograft tumor experiments to evaluate treatment efficacy.
  • RIPK2 expression was upregulated in prostate cancer tissues and associated with poor grading.
  • RIPK2 contributed to docetaxel resistance in multiple prostate cancer cell lines.
  • RIPK2 upregulated P-glycoprotein expression through NF-κB activation.
  • Inhibiting RIPK2 or P-gp increased docetaxel effectiveness in xenograft models.

Cite This Study

Xing et al. (2026) studied this question.

synapsesocial.com/papers/69746126bb9d90c67120b145https://doi.org/10.1371/journal.pone.0341445
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