Evidence map›Paper›PMID 23539448›Full record

ArticleCancer research2013

Androgen receptor-independent function of FoxA1 in prostate cancer metastasis.

Hong-Jian Jin, Jonathan C Zhao, Irene Ogden, Raymond C Bergan, Jindan Yu

Abstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
10.9field-weighted citation impact, top 1% of its field
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

101 citing papers in PubMed, 151 citations in OpenAlex.

  1. Article
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  7. Deep Sequencing Reveals Novel Mutations inInternational journal of molecular sciences · 2025
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  18. SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Article
  20. Article

41 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Hong-Jian JinDivision of Hematology/Oncology, Department of Medicine, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Jonathan C Zhao
Irene Ogden
Raymond C Bergan
Jindan Yu
Northwestern University · USRobert H. Lurie Comprehensive Cancer Center of Northwestern University

Funding

SUPPRESSIVE ROLE OF ANDROGEN RESPONSE GENE CALRETICULIN IN PROSTATE CANCERP50CA090386 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WANG, ZHOU · 2001 to 2013
$25.1M
TRANS-NETWORK PROJECTSU54CA143869 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MARKO, JOHN F · 2009 to 2013
$12.8M
The Role of beta-adrenergic Signaling in Prostate CancerR00CA129565 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI YU, JINDAN · 2010 to 2012
$732k
The Role of beta-adrenergic Signaling in Prostate CancerK99CA129565 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI YU, JINDAN · 2008 to 2009
$310k
NCI NIH HHS K99/R00CA129565NCI NIH HHS P50 CA090386NCI NIH HHS P50CA090386NCI NIH HHS R00 CA129565NCI NIH HHS U54 CA143869NCI NIH HHS U54CA143869
6 · The paper itself

Abstract

FoxA1 (FOXA1) is a pioneering transcription factor of the androgen receptor (AR) that is indispensible for the lineage-specific gene expression of the prostate. To date, there have been conflicting reports on the role of FoxA1 in prostate cancer progression and prognosis. With recent discoveries of recurrent FoxA1 mutations in human prostate tumors, comprehensive understanding of FoxA1 function has become very important. Here, through genomic analysis, we reveal that FoxA1 regulates two distinct oncogenic processes via disparate mechanisms. FoxA1 induces cell growth requiring the AR pathway. On the other hand, FoxA1 inhibits cell motility and epithelial-to-mesenchymal transition (EMT) through AR-independent mechanism directly opposing the action of AR signaling. Using orthotopic mouse models, we further show that FoxA1 inhibits prostate tumor metastasis in vivo. Concordant with these contradictory effects on tumor progression, FoxA1 expression is slightly upregulated in localized prostate cancer wherein cell proliferation is the main feature, but is remarkably downregulated when the disease progresses to metastatic stage for which cell motility and EMT are essential. Importantly, recently identified FoxA1 mutants have drastically attenuated ability in suppressing cell motility. Taken together, our findings illustrate an AR-independent function of FoxA1 as a metastasis inhibitor and provide a mechanism by which recurrent FoxA1 mutations contribute to prostate cancer progression.

Indexed as

AnimalsBlotting, WesternCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression ProfilingGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 3-alphaHumansMaleMiceMice, NudeMutationNeoplasm MetastasisOligonucleotide Array Sequence AnalysisFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaReceptors, Androgen

Identifiers

PMID23539448
PMCPMC3686855
OpenAlexW2114698467

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.