Evidence map›Paper›PMID 40643528›Full record

ArticleCells2025

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

Limiao Liang, Dandan Dong, Jiaxue Sun, Qin Zhang, Xiayun Yang, Gong-Hong Wei, Peng Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Limiao LiangMOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai 200032, China.
Dandan DongMOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai 200032, China.
Jiaxue SunMOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai 200032, China.
Qin ZhangDisease Networks Research Unit, Faculty of Biochemistry and Molecular Medicine & Biocenter Oulu, University of Oulu, 90220 Oulu, Finland.ORCID 0000-0003-3467-4241
Xiayun YangDisease Networks Research Unit, Faculty of Biochemistry and Molecular Medicine & Biocenter Oulu, University of Oulu, 90220 Oulu, Finland.
Gong-Hong WeiMOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai 200032, China.ORCID 0000-0001-6546-9334
Peng ZhangMOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai 200032, China.ORCID 0000-0002-6389-7404

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia is a hallmark of aggressive prostate cancer, but how it disrupts lineage-specific transcriptional programs to drive progression remains unclear. Here, we identify the HIF1α-PHD1-FOXA1 axis as a critical mediator of hypoxic adaptation and androgen signaling suppression. Using genome-wide profiling, we demonstrate that hypoxia reprograms HIF1α chromatin occupancy, shifting its cooperation from AR to FOXA1. Mechanistically, HIF1α physically interacts with FOXA1, destabilizing it via PHD1-mediated hydroxylation-a previously unrecognized post-translational regulatory node. Under hypoxia, loss of FOXA1 attenuates androgen-responsive transcription while activating hypoxia-inducible genes, demonstrating a dual role for this axis in hypoxia adaptation and prostate cancer progression. Genetic or pharmacological disruption of HIF1α-PHD1-FOXA1 impairs prostate cancer proliferation and migration, underscoring its translational relevance. Our findings establish oxygen-dependent FOXA1 degradation as a linchpin connecting microenvironmental stress to transcriptional plasticity in advanced prostate cancer, offering new therapeutic avenues.

Indexed as

AndrogensCellular ReprogrammingHepatocyte Nuclear Factor 3-alphaHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesProstatic NeoplasmsSignal TransductionAnimalsCell HypoxiaCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMaleAndrogensEGLN1 protein, humanFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline Dioxygenasescistrome reprogrammingFOXA1HIF1αPHD1prostate cancer

Identifiers

PMID40643528
PMCPMC12248476

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.