Evidence map›Paper›PMID 26175158›Full record

ArticleThe Journal of biological chemistry2015

The Deubiquitinating Enzyme USP7 Regulates Androgen Receptor Activity by Modulating Its Binding to Chromatin.

Shu-Ting Chen, Maiko Okada, Ryuichiro Nakato, Kosuke Izumi, Masashige Bando, Katsuhiko Shirahige

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. USP11 promotes prostate cancer progression by up-regulating AR and c-Myc activity.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Article
  6. Review
  7. Deubiquitylating Enzymes in Cancer and Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
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  17. Article
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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

6 authors at 1 institution in 1 country.

Shu-Ting ChenFrom the Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032 and.
Maiko Okadathe Department of Translational Oncology, St. Marianna University Graduate School of Medicine, Kawasaki 216-8511, Japan.
Ryuichiro NakatoFrom the Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032 and.
Kosuke IzumiFrom the Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032 and.
Masashige BandoFrom the Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032 and.
Katsuhiko ShirahigeFrom the Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032 and kshirahi@iam.u-tokyo.ac.jp.
St. Marianna University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The androgen receptor (AR), a nuclear receptor superfamily transcription factor, plays a key role in prostate cancer. AR signaling is the principal target for prostate cancer treatment, but current androgen-deprivation therapies cannot completely abolish AR signaling because of the heterogeneity of prostate cancers. Therefore, unraveling the mechanism of AR reactivation in androgen-depleted conditions can identify effective prostate cancer therapeutic targets. Increasing evidence indicates that AR activity is mediated by the interplay of modifying/demodifying enzymatic co-regulators. To better understand the mechanism of AR transcriptional activity regulation, we used antibodies against AR for affinity purification and identified the deubiquitinating enzyme ubiquitin-specific protease 7, USP7 as a novel AR co-regulator in prostate cancer cells. We showed that USP7 associates with AR in an androgen-dependent manner and mediates AR deubiquitination. Sequential ChIP assays indicated that USP7 forms a complex with AR on androgen-responsive elements of target genes upon stimulation with the androgen 5α-dihydrotestosterone. Further investigation indicated that USP7 is necessary to facilitate androgen-activated AR binding to chromatin. Transcriptome profile analysis of USP7-knockdown LNCaP cells also revealed the essential role of USP7 in the expression of a subset of androgen-responsive genes. Hence, inhibition of USP7 represents a compelling therapeutic strategy for the treatment of prostate cancer.

Indexed as

AndrogensCell Line, TumorCell ProliferationChromatinGene Expression Regulation, NeoplasticHumansMaleProstatic NeoplasmsProtein BindingReceptors, AndrogenResponse ElementsUbiquitinationUbiquitin-Specific Peptidase 7Ubiquitin ThiolesteraseAndrogensAR protein, humanChromatinReceptors, AndrogenUbiquitin-Specific Peptidase 7Ubiquitin ThiolesteraseUSP7 protein, humanandrogen receptorgene transcriptionprostate cancertranscriptional coactivatorubiquitin-dependent protease

Identifiers

PMID26175158
PMCPMC4571893
OpenAlexW1899841688

What OpenQuestion holds

Textmetadata
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.