Evidence map›Paper›PMID 24292673›Full record

ArticleOncogene2014

ZRF1 controls the retinoic acid pathway and regulates leukemogenic potential in acute myeloid leukemia.

S Demajo, I Uribesalgo, A Gutiérrez, C Ballaré, S Capdevila, M Roth, J Zuber, J Martín-Caballero, L Di Croce

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  10. A Cyclin D1-Dependent Transcriptional Program Predicts Clinical Outcome in Mantle Cell Lymphoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
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  15. Silencing of ZRF1 impedes survival of estrogen receptor positive MCF-7 cells and potentiates the effect of curcumin.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

9 authors at 3 institutions in 2 countries.

S Demajo1] Centre de Regulació Genòmica (CRG), Barcelona, Spain [2] UPF, Barcelona, Spain.
I Uribesalgo1] Centre de Regulació Genòmica (CRG), Barcelona, Spain [2] UPF, Barcelona, Spain.
A Gutiérrez1] Centre de Regulació Genòmica (CRG), Barcelona, Spain [2] UPF, Barcelona, Spain.
C Ballaré1] Centre de Regulació Genòmica (CRG), Barcelona, Spain [2] UPF, Barcelona, Spain.
S CapdevilaUnidad de Animal de Laboratorio, PRBB, Barcelona, Spain.
M RothInstitute of Molecular Pathology (IMP), Vienna, Austria.
J ZuberInstitute of Molecular Pathology (IMP), Vienna, Austria.
J Martín-CaballeroUnidad de Animal de Laboratorio, PRBB, Barcelona, Spain.
L Di Croce1] Centre de Regulació Genòmica (CRG), Barcelona, Spain [2] UPF, Barcelona, Spain [3] Institució Catalana de Recerca i Estudis Avançats (ICREA), Barcelona, Spain.
Centre for Genomic Regulation · ESResearch Institute of Molecular Pathology · ATFC Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is frequently linked to epigenetic abnormalities and deregulation of gene transcription, which lead to aberrant cell proliferation and accumulation of undifferentiated precursors. ZRF1, a recently characterized epigenetic factor involved in transcriptional regulation, is highly overexpressed in human AML, but it is not known whether it plays a role in leukemia progression. Here, we demonstrate that ZRF1 depletion decreases cell proliferation, induces apoptosis and enhances cell differentiation in human AML cells. Treatment with retinoic acid (RA), a differentiating agent currently used to treat certain AMLs, leads to a functional switch of ZRF1 from a negative regulator to an activator of differentiation. At the molecular level, ZRF1 controls the RA-regulated gene network through its interaction with the RA receptor α (RARα) and its binding to RA target genes. Our genome-wide expression study reveals that ZRF1 regulates the transcription of nearly half of RA target genes. Consistent with our in vitro observations that ZRF1 regulates proliferation, apoptosis, and differentiation, ZRF1 depletion strongly inhibits leukemia progression in a xenograft mouse model. Finally, ZRF1 knockdown cooperates with RA treatment in leukemia suppression in vivo. Taken together, our data reveal that ZRF1 is a key transcriptional regulator in leukemia progression and suggest that ZRF1 inhibition could be a novel strategy to be explored for AML treatment.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBlotting, WesternCell DifferentiationCell Line, TumorCell ProliferationDisease ProgressionDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansImmunoprecipitationLeukemia, Myeloid, AcuteMiceMice, SCIDMolecular ChaperonesAntineoplastic AgentsDNA-Binding ProteinsDNAJC2 protein, humanMolecular ChaperonesOncogene ProteinsRNA-Binding ProteinsTretinoin

Identifiers

PMID24292673
OpenAlexW1978560193

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.