Evidence map›Paper›PMID 36275699›Full record

ArticleFrontiers in immunology2022

UCP2 silencing restrains leukemia cell proliferation through glutamine metabolic remodeling.

Tiphaine Sancerni, Ophélie Renoult, Angèle Luby, Cédric Caradeuc, Véronique Lenoir, Mikael Croyal, Céline Ransy, Esther Aguilar, Catherine Postic, Gildas Bertho and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
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  6. Dysfunctional glycolysis-UCP2-fatty acid oxidation promotes CTLA4Molecular medicine (Cambridge, Mass.) · 2025
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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

14 authors at 8 institutions in 2 countries.

Tiphaine SancerniUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Ophélie RenoultNantes Université, INSERM, CNRS, CRCI2NA, Nantes, France.
Angèle LubyUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Cédric CaradeucUniversité Paris Cité, CNRS UMR8601, Paris, France.
Véronique LenoirUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Mikael CroyalNantes Université, INSERM, CNRS, CRCI2NA, Nantes, France.
Céline RansyUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Esther AguilarAsociación Española Contra el Cáncer (AECC), Fundación Científica AECC, Madrid, Spain.
Catherine PosticUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Gildas BerthoUniversité Paris Cité, CNRS UMR8601, Paris, France.
Renaud DentinUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Carina Prip-BuusUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Claire PecqueurNantes Université, INSERM, CNRS, CRCI2NA, Nantes, France.
Marie-Clotilde Alves-GuerraUniversité Paris Cité, CNRS, INSERM, Institut Cochin, Paris, France.
Centre National de la Recherche Scientifique · FRInstitut Cochin · FRCentre de Recherche en Cancérologie et Immunologie Intégrée Nantes Angers · FRUniversité Paris Cité · FRAsociación Española Contra el Cáncer · ESInserm · FRNantes Université · FRSorbonne Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy derived from early T cell progenitors. Since relapsed T-ALL is associated with a poor prognosis improving initial treatment of patients is essential to avoid resistant selection of T-ALL. During initiation, development, metastasis and even in response to chemotherapy, tumor cells face strong metabolic challenges. In this study, we identify mitochondrial UnCoupling Protein 2 (UCP2) as a tricarboxylic acid (TCA) cycle metabolite transporter controlling glutamine metabolism associated with T-ALL cell proliferation. In T-ALL cell lines, we show that UCP2 expression is controlled by glutamine metabolism and is essential for their proliferation. Our data show that T-ALL cell lines differ in their substrate dependency and their energetic metabolism (glycolysis and oxidative). Thus, while UCP2 silencing decreases cell proliferation in all leukemia cells, it also alters mitochondrial respiration of T-ALL cells relying on glutamine-dependent oxidative metabolism by rewiring their cellular metabolism to glycolysis. In this context, the function of UCP2 in the metabolite export of malate enables appropriate TCA cycle to provide building blocks such as lipids for cell growth and mitochondrial respiration. Therefore, interfering with UCP2 function can be considered as an interesting strategy to decrease metabolic efficiency and proliferation rate of leukemia cells.

Indexed as

GlutaminePrecursor T-Cell Lymphoblastic Leukemia-LymphomaCell ProliferationHumansLipidsMalatesTricarboxylic AcidsUncoupling Protein 2GlutamineLipidsMalatesTricarboxylic AcidsUCP2 protein, humanUncoupling Protein 2glutamineleukemiametabolism rewiringmetabolite carriermitochondriaUCP2

Identifiers

PMID36275699
PMCPMC9582289
OpenAlexW4303186318

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.