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Androgen Receptor-Induced Lactoferrin Accelerates Prostate Tumorigenesis Through Modulating Ferroptosis.

Can Liu1,2,3,4,5, Qiu Peng1, Xiaoyue Zhang1,2,4

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Lactoferrin (LF) surprisingly drives prostate cancer by suppressing ferroptosis via an androgen receptor (AR) axis. Targeting this LF-AR-ferroptosis pathway offers a novel therapeutic strategy for prostate cancer.

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TRAMP mouse modelandrogen receptorferroptosislactoferrinprostate cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Lactoferrin (LF) is highly expressed in the prostate, suggesting a key physiological role.
  • While LF is tumor-suppressive in other cancers, its function in prostate cancer is unclear.

Purpose of the Study:

  • To investigate the role of lactoferrin in prostate cancer.
  • To elucidate the mechanism of lactoferrin's function in prostate cancer through the androgen receptor (AR)-LF-ferroptosis axis.

Main Methods:

  • Utilized Lf knockout TRAMP mouse models, proteomics, TCGA-PARD data, and single-cell RNA-seq.
  • Investigated AR binding to the LF promoter and its effect on ferritin expression and ferroptosis.
  • Conducted preclinical studies using LF knockdown, ferroptosis inducers (IKE), and AR inhibitors (enzalutamide) in xenograft models.

Main Results:

  • AR directly upregulates LF expression, which suppresses ferroptosis by increasing ferritin and inhibiting p53-ALOX12.
  • LF deficiency delayed tumor progression and increased ferroptosis in TRAMP mice; iron supplementation accelerated cancer, an effect reversed by LF knockout.
  • Lactoferrin protects prostate cancer cells from iron-induced ferroptosis by maintaining iron-redox homeostasis.

Conclusions:

  • Lactoferrin acts as an AR-regulated suppressor of ferroptosis in prostate cancer.
  • LF regulates prostate cancer's dependence on iron metabolism.
  • LF is a potential therapeutic target for exploiting prostate cancer's iron-metabolic vulnerability.