Evidence map›Paper›PMID 14645547›Full record

ArticleMolecular and cellular biology2003

Growth suppression by acute promyelocytic leukemia-associated protein PLZF is mediated by repression of c-myc expression.

Melanie J McConnell, Nathalie Chevallier, Windy Berkofsky-Fessler, Jena M Giltnane, Rupal B Malani, Louis M Staudt, Jonathan D Licht

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
2.3field-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

72 citing papers in PubMed, 122 citations in OpenAlex.

  1. Review
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  13. Enhanced oxidative phosphorylation in NKT cells is essential for their survival and function.Proceedings of the National Academy of Sciences of the United States of America · 2019
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  14. Low Expression of the Androgen-Induced Tumor Suppressor GeneCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019
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12 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

7 authors at 2 institutions in 2 countries.

Melanie J McConnellDivision of Hematology/Oncology, Department of Medicine, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
Nathalie Chevallier
Windy Berkofsky-Fessler
Jena M Giltnane
Rupal B Malani
Louis M Staudt
Jonathan D Licht
Icahn School of Medicine at Mount Sinai · USNational Cancer Institute · MY

Funding

The PLZF Protein of t(11;17)-Promyelocytic LeukemiaR01CA059936 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LICHT, JONATHAN · 1993 to 2007
$2.9M
NCI NIH HHS CA 59936NCI NIH HHS R01 CA059936
6 · The paper itself

Abstract

The transcriptional repressor PLZF was identified by its translocation with retinoic acid receptor alpha in t(11;17) acute promyelocytic leukemia (APL). Ectopic expression of PLZF leads to cell cycle arrest and growth suppression, while disruption of normal PLZF function is implicated in the development of APL. To clarify the function of PLZF in cell growth and survival, we used an inducible PLZF cell line in a microarray analysis to identify the target genes repressed by PLZF. One prominent gene identified was c-myc. The array analysis demonstrated that repression of c-myc by PLZF led to a reduction in c-myc-activated transcripts and an increase in c-myc-repressed transcripts. Regulation of c-myc by PLZF was shown to be both direct and reversible. An interaction between PLZF and the c-myc promoter could be detected both in vitro and in vivo. PLZF repressed the wild-type c-myc promoter in a reporter assay, dependent on the integrity of the binding site identified in vitro. PLZF binding in vivo was coincident with a decrease in RNA polymerase occupation of the c-myc promoter, indicating that repression occurred via a reduction in the initiation of transcription. Finally, expression of c-myc reversed the cell cycle arrest induced by PLZF. These data suggest that PLZF expression maintains a cell in a quiescent state by repressing c-myc expression and preventing cell cycle progression. Loss of this repression through the translocation that occurs in t(11;17) would have serious consequences for cell growth control.

Indexed as

Genes, mycApoptosisBase SequenceBinding SitesCell CycleCell DivisionChromosomes, Human, Pair 11Chromosomes, Human, Pair 17DNA-Binding ProteinsDNA, ComplementaryGene ExpressionHumansKruppel-Like Transcription FactorsLeukemia, Promyelocytic, AcutePromoter Regions, GeneticPromyelocytic Leukemia Zinc Finger ProteinDNA-Binding ProteinsDNA, ComplementaryKruppel-Like Transcription FactorsPromyelocytic Leukemia Zinc Finger ProteinRepressor ProteinsTranscription FactorsZBTB16 protein, human

Identifiers

PMID14645547
PMCPMC309637
OpenAlexW2155508906

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.