Evidence map›Paper›PMID 30479348›Full record

ArticleNature communications2018

TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression.

Ka-Wing Fong, Jonathan C Zhao, Bing Song, Bin Zheng, Jindan Yu

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
3.9field-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

88 citing papers in PubMed, 150 citations in OpenAlex.

  1. Review
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  5. High-throughput screening identifies a critical role of the SPOP-PABPC1 axis in lung adenocarcinoma progression.Proceedings of the National Academy of Sciences of the United States of America · 2026
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28 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 1 institution in 1 country.

Ka-Wing FongDivision of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Jonathan C ZhaoDivision of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Bing SongDivision of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Bin ZhengDivision of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Jindan YuDivision of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. jindan-yu@northwestern.edu.
Northwestern University · US

Funding

Targeting FOXA1-downstream pathways: a novel therapeutic strategy for castration-resistant prostate cancerP50CA180995 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ABDULKADIR, SARKI A., HUSSAIN, MAHA H · 2015 to 2025
$19.9M
The Role of NOV (CCN3) in Prostate Cancer ProgressionR01CA172384 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI YU, JINDAN · 2013 to 2017
$1.6M
Genomics and bioinformatics analysis to understand castration-resistant prostate cancerR50CA211271 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ZHAO, CHANGSHENG · 2016 to 2020
$701k
NCI NIH HHS P50 CA180995NCI NIH HHS R01 CA172384NCI NIH HHS R50 CA211271
6 · The paper itself

Abstract

TRIM24 is an effector substrate of the E3 ubiquitin ligase adaptor SPOP and becomes stabilized in prostate cancer (PCa) with SPOP mutations. However, how TRIM24 protein is regulated in the vast majority of SPOP-wildtype PCa is unknown. Here we report TRIM28 as a critical upstream regulator of TRIM24. TRIM28 protein interacts with TRIM24 to prevent its ubiquitination and degradation by SPOP. Further, TRIM28 facilitates TRIM24 occupancy on the chromatin and, like TRIM24, augments AR signaling. TRIM28 promotes PCa cell proliferation in vitro and xenograft tumor growth in vivo. Importantly, TRIM28 is upregulated in aggressive PCa and associated with elevated levels of TRIM24 and worse clinical outcome. TRIM24 and AR coactivated gene signature of SPOP-mutant PCa is similarly activated in human PCa with high TRIM28 expression. Taken together, this study provides a novel mechanism to broad TRIM24 protein stabilization and establishes TRIM28 as a promising therapeutic target.

Indexed as

Disease ProgressionProteolysisCarcinogenesisCarrier ProteinsCell Line, TumorHumansMaleNuclear ProteinsProstatic NeoplasmsProtein BindingProtein StabilityReceptors, AndrogenRepressor ProteinsSignal TransductionTranscription, GeneticTripartite Motif-Containing Protein 28Carrier ProteinsNuclear ProteinsReceptors, AndrogenRepressor ProteinsSPOP protein, humanTRIM24 protein, humanTRIM28 protein, humanTripartite Motif-Containing Protein 28

Identifiers

PMID30479348
PMCPMC6258673
OpenAlexW2901276642

What OpenQuestion holds

Textmetadata
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.