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HIF1α-PHD1-FOXA1 Axis Orchestrates Hypoxic Reprogramming and Androgen Signaling Suppression in Prostate Cancer.

Limiao Liang1, Dandan Dong1, Jiaxue Sun1

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Summary
This summary is machine-generated.

Hypoxia in prostate cancer disrupts gene programs via the HIF1α-PHD1-FOXA1 axis. This pathway links low oxygen to cancer progression and offers new therapeutic targets.

Keywords:
FOXA1HIF1αPHD1cistrome reprogrammingprostate cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Hypoxia is a key characteristic of aggressive prostate cancer.
  • The mechanisms by which hypoxia drives prostate cancer progression by altering transcriptional programs are not fully understood.

Purpose of the Study:

  • To identify the molecular mechanisms linking hypoxia to prostate cancer progression.
  • To investigate the role of the HIF1α-PHD1-FOXA1 axis in hypoxic adaptation and androgen signaling suppression.

Main Methods:

  • Genome-wide profiling to analyze HIF1α chromatin occupancy under hypoxia.
  • Co-immunoprecipitation to assess physical interactions between HIF1α and FOXA1.
  • Assessment of androgen-responsive and hypoxia-inducible gene expression.
  • Evaluation of the effects of disrupting the HIF1α-PHD1-FOXA1 axis on prostate cancer cell behavior.

Main Results:

  • Hypoxia reprograms HIF1α to cooperate with FOXA1 instead of AR.
  • HIF1α physically interacts with FOXA1, leading to its destabilization through PHD1-mediated hydroxylation.
  • Loss of FOXA1 under hypoxia attenuates androgen signaling and activates hypoxia-inducible genes.
  • Disruption of the HIF1α-PHD1-FOXA1 axis inhibits prostate cancer cell proliferation and migration.

Conclusions:

  • The HIF1α-PHD1-FOXA1 axis is a critical mediator of hypoxic adaptation in prostate cancer.
  • Oxygen-dependent FOXA1 degradation connects microenvironmental stress to transcriptional changes in advanced prostate cancer.
  • Targeting this axis presents a promising therapeutic strategy for prostate cancer.