Evidence map›Paper›PMID 34057812›Full record

ArticleMolecular oncology2022

FKBP51 and FKBP52 regulate androgen receptor dimerization and proliferation in prostate cancer cells.

Keisuke Maeda, Makoto Habara, Mitsuyasu Kawaguchi, Hiroaki Matsumoto, Shunsuke Hanaki, Takahiro Masaki, Yuki Sato, Hideyasu Matsuyama, Kazuki Kunieda, Hidehiko Nakagawa and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

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  6. Genome-wide identification and expression analyses ofPhysiology and molecular biology of plants : an international journal of functional plant biology · 2024
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  20. FKBP52 and FKBP51 differentially regulate the stability of estrogen receptor in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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

11 authors at 2 institutions in 1 country.

Keisuke MaedaDepartment of Biochemistry, Joint Faculty of Veterinary Science, Yamaguchi University, Japan.ORCID 0000-0002-5278-4500
Makoto HabaraDepartment of Biochemistry, Joint Faculty of Veterinary Science, Yamaguchi University, Japan.ORCID 0000-0001-6418-1291
Mitsuyasu KawaguchiGraduate School of Pharmaceutical Sciences, Nagoya City University, Japan.
Hiroaki MatsumotoDepartment of Urology, Graduate School of Medicine, Yamaguchi University, Ube, Japan.
Shunsuke HanakiDepartment of Biochemistry, Joint Faculty of Veterinary Science, Yamaguchi University, Japan.
Takahiro MasakiDepartment of Biochemistry, Joint Faculty of Veterinary Science, Yamaguchi University, Japan.
Yuki SatoDepartment of Biochemistry, Joint Faculty of Veterinary Science, Yamaguchi University, Japan.
Hideyasu MatsuyamaDepartment of Urology, Graduate School of Medicine, Yamaguchi University, Ube, Japan.
Kazuki KuniedaGraduate School of Pharmaceutical Sciences, Nagoya City University, Japan.
Hidehiko NakagawaGraduate School of Pharmaceutical Sciences, Nagoya City University, Japan.
Midori ShimadaDepartment of Biochemistry, Joint Faculty of Veterinary Science, Yamaguchi University, Japan.ORCID 0000-0002-2718-8600
Yamaguchi University · JPNagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The growth of prostate cancer is dependent on the androgen receptor (AR), which serves as a ligand-specific transcription factor. Although two immunophilins, FKBP51 and FKBP52, are known to regulate AR activity, the precise mechanism remains unclear. We found that depletion of either FKBP51 or FKBP52 reduced AR dimer formation, chromatin binding, and phosphorylation, suggesting defective AR signaling. Furthermore, the peptidyl-prolyl cis/trans isomerase activity of FKBP51 was found to be required for AR dimer formation and cancer cell growth. Treatment of prostate cancer cells with FK506, which binds to the FK1 domain of FKBPs, or with MJC13, an inhibitor of FKBP52-AR signaling, also inhibited AR dimer formation. Finally, elevated expression of FKBP52 was associated with a higher rate of prostate-specific antigen recurrence in patients with prostate cancer. Collectively, these results suggest that FKBP51 and FKBP52 might be promising targets for prostate cancer treatment through the inhibition of AR dimer formation.

Indexed as

Prostatic NeoplasmsReceptors, AndrogenCell ProliferationDimerizationHumansMaleTacrolimus Binding Protein 5Tacrolimus Binding ProteinsReceptors, Androgentacrolimus binding protein 4Tacrolimus Binding Protein 5Tacrolimus Binding Proteinsimmunophilinpeptidyl-prolyl cis/trans isomeraseprostate cancersteroid receptor

Identifiers

PMID34057812
PMCPMC8847985
OpenAlexW3164344078

What OpenQuestion holds

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LicenceCC BY
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.