Association between the anticancer efficacy of cabazitaxel and toll-like receptor 4 mediating signaling pathways in metastatic castration-resistant prostate cancer cells

Hum Exp Toxicol. 2021 Jul;40(7):1122-1129. doi: 10.1177/0960327120984209. Epub 2020 Dec 31.

Abstract

Background: We evaluated the effect of cabazitaxel (CAB) as a third-line taxane on Toll-like receptor 4 (TLR4)-mediated signaling pathways, especially NF-κB activity, in metastatic castration-resistant prostate cancer (mCRPC) cells.

Methods: CAB cytotoxicity was determined by WST-1 assay. To assess the relationship between CAB efficacy and TLR4 signaling pathways, RT-PCR, western blot and immunofluorescence analysis were performed. Additionally, CAB-mediated apoptotic cell death was assessed by Annexin V and RT-PCR analysis.

Results: Our results demonstrated that CAB exerted considerably cytotoxic and apoptotic effects on PC-3 mCRPC cells (p < 0.05). CAB treatment altered TLR4 expression level in a dose-dependent manner. Furthermore, 1 nM CAB treatment significantly induced NF-κB activity through p65 nuclear localization and increased the expression level of caspase-3, Bax and p53. Interestingly, total apoptotic cell death and IRF3 protein levels were increased at 5 nM concentration of CAB despite a decrease in the levels of both NF-κB and pro-apoptotic genes.

Conclusions: Therefore, NF-κB activity may be a potential target for the efficacy of CAB in mCRPC cells.

Keywords: Metastatic castration-resistant prostate cancer; NF-κB activity; apoptosis; cabazitaxel; toll-like receptor 4.

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Apoptosis / drug effects*
  • Cell Survival / drug effects
  • Cells, Cultured / drug effects
  • Humans
  • Male
  • Prostatic Neoplasms, Castration-Resistant / drug therapy*
  • Prostatic Neoplasms, Castration-Resistant / physiopathology
  • Signal Transduction / drug effects*
  • Taxoids / therapeutic use*
  • Taxoids / toxicity*
  • Toll-Like Receptor 4 / therapeutic use*
  • Treatment Outcome

Substances

  • Antineoplastic Agents
  • Taxoids
  • Toll-Like Receptor 4