Evidence map›Paper›PMID 22330138›Full record

ArticleOncogene2012

The SRA protein UHRF1 promotes epigenetic crosstalks and is involved in prostate cancer progression.

F Babbio, C Pistore, L Curti, I Castiglioni, P Kunderfranco, L Brino, P Oudet, R Seiler, G N Thalman, E Roggero and 7 more

Abstract read
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In one paragraph

Article in Oncogene, 2012. 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
5.0field-weighted citation impact, top 4% 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, 133 citations in OpenAlex.

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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

17 authors at 6 institutions in 3 countries.

F BabbioDepartment of Structural and Functional Biology, University of Insubria, Via A da Giussano 12, Busto Arsizio, Italy.
C Pistore
L Curti
I Castiglioni
P Kunderfranco
L Brino
P Oudet
R Seiler
G N Thalman
E Roggero
M Sarti
S Pinton
M Mello-Grand
G Chiorino
C V Catapano
G M Carbone
I M Bonapace
Institute of Oncology Research · CHUniversity of Insubria · ITFondazione Edo ed Elvo Tempia · ITInstitut de génétique et de biologie moléculaire et cellulaire · FRUniversity Hospital of Bern · CHCancéropôle Est · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic silencing of tumour suppressor genes is an important mechanism involved in cell transformation and tumour progression. The Set and RING-finger-associated domain-containing protein UHRF1 might be an important link between different epigenetic pathways. Here, we report that UHRF1 is frequently overexpressed in human prostate tumours and has an important role in prostate cancer pathogenesis and progression. Analysis of human prostate cancer samples by microarrays and immunohistochemistry showed increased expression of UHRF1 in about half of the cases. Moreover, UHRF1 expression was associated with reduced overall survival after prostatectomy in patients with organ-confined prostate tumours (P < 0.0001). UHRF1 expression was negatively correlated with several tumour suppressor genes and positively with the histone methyltransferase (HMT) EZH2 both in prostate tumours and cell lines. UHRF1 knockdown reduced proliferation, clonogenic capability and anchorage-independent growth of prostate cancer cells. Depletion of UHRF1 resulted in reactivation of several tumour suppressor genes. Gene reactivation upon UHRF1 depletion was associated with changes in histone H3K9 methylation, acetylation and DNA methylation, and impaired binding of the H3K9 HMT Suv39H1 to the promoter of silenced genes. Co-immunoprecipitation experiments showed direct interaction between UHRF1 and Suv39H1. Our data support the notion that UHRF1, along with Suv39H1 and DNA methyltransferases, contributes to epigenetic gene silencing in prostate tumours. This could represent a parallel and convergent pathway to the H3K27 methylation catalyzed by EZH2 to synergistically promote inactivation of tumour suppressor genes. Deregulated expression of UHRF1 is involved in the prostate cancer pathogenesis and might represent a useful marker to distinguish indolent cancer from those at high risk of lethal progression.

Indexed as

AcetylationCCAAT-Enhancer-Binding ProteinsCell Growth ProcessesCell Line, TumorDisease ProgressionDNA-Binding ProteinsDNA MethylationEnhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticGene Expression Regulation, NeoplasticGene SilencingGenes, Tumor SuppressorHEK293 CellsHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHistonesCCAAT-Enhancer-Binding ProteinsDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHistonesPolycomb Repressive Complex 2Ubiquitin-Protein LigasesUHRF1 protein, human

Identifiers

PMID22330138
OpenAlexW2064522668

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.