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Metabolic vulnerabilities in advanced prostate cancer: the interplay of ferroptosis, cuproptosis, and the

Farzaneh Motafeghi1, Parham Mortazavi2, Mohammad Hossein Hosseinzadeh3

  • 1Reproductive Endocrinology Research Center, Research Institute for Endocrine Molecular Biology, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. farzaneh.motafeghi@gmail.com.

Medical Oncology (Northwood, London, England)
|June 12, 2026
PubMed

Insights

Targeting ferroptosis and cuproptosis offers new hope for advanced prostate cancer by exploiting metal-dependent vulnerabilities. This approach aims to overcome resistance and improve outcomes in metastatic castration-resistant prostate cancer (mCRPC).

Area of Science:

  • Oncology
  • Biochemistry
  • Cell Death Mechanisms

Background:

  • Advanced prostate cancer, especially metastatic castration-resistant prostate cancer (mCRPC), poses significant challenges due to resistance to apoptosis.
  • Alternative cell death pathways, ferroptosis and cuproptosis, are emerging as critical therapeutic targets.
  • These metal-dependent cell death modalities are intricately linked to mitochondrial function, lipid metabolism, and the tumor microenvironment.

Purpose of the Study:

  • To review the biochemical basis of ferroptosis and cuproptosis in the context of advanced prostate cancer.
  • To explore the interplay between metal ion homeostasis, antioxidant pathways (NRF2/GPX4), and inflammation.
  • To highlight the potential of novel therapeutic strategies and biomarkers for precision oncology.

Main Methods:

  • Comprehensive literature review synthesizing current multi-omics data.
  • Evaluation of pharmacological strategies, including nanotherapies and theranostic radiopharmaceuticals.
  • Analysis of the role of the NRF2/GPX4 axis and inflammatory signaling in metal ion homeostasis.

Main Results:

  • Ferroptosis and cuproptosis represent exploitable vulnerabilities in advanced prostate cancer.
  • Mitochondrial bioenergetics, lipid remodeling, and the tumor microenvironment significantly influence these pathways.
  • The NRF2/GPX4 axis and inflammatory signaling modulate metal ion homeostasis, impacting cell death sensitivity.

Conclusions:

  • Targeting ferroptosis and cuproptosis holds promise for overcoming therapeutic resistance in advanced prostate cancer.
  • Development of predictive biomarkers and rational combinatorial therapies is crucial for clinical success.
  • Integrating mechanistic insights with precision oncology strategies is essential for improving patient outcomes in mCRPC.
Keywords:
Castration-Resistant Prostate Cancer (CRPC)CuproptosisFerroptosisOxidative stressPrecision oncologyProstate carcinomaTheranosticsTumor microenvironment

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