Evidence map›Paper›PMID 25034783›Full record

ArticleCell death and differentiation2014

p62/SQSTM1 upregulation constitutes a survival mechanism that occurs during granulocytic differentiation of acute myeloid leukemia cells.

A Trocoli, P Bensadoun, E Richard, G Labrunie, F Merhi, A M Schläfli, D Brigger, S Souquere, G Pierron, J-M Pasquet and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.

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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

15 authors at 7 institutions in 2 countries.

A Trocoli1] INSERM U916 VINCO, Institut Bergonié, 229, cours de l'Argonne 33076 Bordeaux Cedex, France [2] Université Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux cedex, France.
P Bensadoun1] INSERM U916 VINCO, Institut Bergonié, 229, cours de l'Argonne 33076 Bordeaux Cedex, France [2] Université Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux cedex, France.
E Richard1] INSERM U916 VINCO, Institut Bergonié, 229, cours de l'Argonne 33076 Bordeaux Cedex, France [2] Université Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux cedex, France.
G Labrunie1] INSERM U916 VINCO, Institut Bergonié, 229, cours de l'Argonne 33076 Bordeaux Cedex, France [2] Université Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux cedex, France.
F Merhi1] INSERM U916 VINCO, Institut Bergonié, 229, cours de l'Argonne 33076 Bordeaux Cedex, France [2] Université Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux cedex, France.
A M SchläfliDivision of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
D BriggerDivision of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
S SouquereUMR 8122, CNRS - IGR - Université Paris-XI, Villejuif, France.
G PierronUMR 8122, CNRS - IGR - Université Paris-XI, Villejuif, France.
J-M PasquetINSERM U1035, Université Bordeaux, Bordeaux, France.
P Soubeyran1] INSERM U916 VINCO, Institut Bergonié, 229, cours de l'Argonne 33076 Bordeaux Cedex, France [2] Université Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux cedex, France.
J Reiffers1] INSERM U916 VINCO, Institut Bergonié, 229, cours de l'Argonne 33076 Bordeaux Cedex, France [2] Université Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux cedex, France.
E Ségal-BendirdjianINSERM UMR-S 1007, Cellular Homeostasis and Cancer, Université Paris Descartes, Sorbonne Paris Cité, 45 rue des Saints-Pères, 75006, Paris, France.
M P TschanDivision of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.
M Djavaheri-Mergny1] INSERM U916 VINCO, Institut Bergonié, 229, cours de l'Argonne 33076 Bordeaux Cedex, France [2] Université Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux cedex, France.
Inserm · FRInstitut Bergonié · FRUniversity of Bern · CHUniversité de Bordeaux · FRCentre National de la Recherche Scientifique · FRSorbonne Paris Cité · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p62/SQSTM1 adapter protein has an important role in the regulation of several key signaling pathways and helps transport ubiquitinated proteins to the autophagosomes and proteasome for degradation. Here, we investigate the regulation and roles of p62/SQSTM1 during acute myeloid leukemia (AML) cell maturation into granulocytes. Levels of p62/SQSTM1 mRNA and protein were both significantly increased during all-trans retinoic acid (ATRA)-induced differentiation of AML cells through a mechanism that depends on NF-κB activation. We show that this response constitutes a survival mechanism that prolongs the life span of mature AML cells and mitigates the effects of accumulation of aggregated proteins that occurs during granulocytic differentiation. Interestingly, ATRA-induced p62/SQSTM1 upregulation was impaired in maturation-resistant AML cells but was reactivated when differentiation was restored in these cells. Primary blast cells of AML patients and CD34(+) progenitors exhibited significantly lower p62/SQSTM1 mRNA levels than did mature granulocytes from healthy donors. Our results demonstrate that p62/SQSTM1 expression is upregulated in mature compared with immature myeloid cells and reveal a pro-survival function of the NF-κB/SQSTM1 signaling axis during granulocytic differentiation of AML cells. These findings may help our understanding of neutrophil/granulocyte development and will guide the development of novel therapeutic strategies for refractory and relapsed AML patients with previous exposure to ATRA.

Indexed as

Adaptor Proteins, Signal TransducingCell Line, TumorCell SurvivalCell Transformation, NeoplasticGene ExpressionGene Expression Regulation, LeukemicGranulocytesHumansLeukemia, Myeloid, AcuteSequestosome-1 ProteinTretinoinUbiquitinationUp-RegulationAdaptor Proteins, Signal TransducingSequestosome-1 ProteinSQSTM1 protein, humanTretinoin

Identifiers

PMID25034783
PMCPMC4227143
OpenAlexW2083193063

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.