Evidence map›Paper›PMID 42401573›Full record

ArticleCell death & disease2026

The alternative NF-κB RelB subunit is a novel critical sensor of lipid metabolism to promote tumor development.

T Becquard, C Benatar, C Bretot, B Eluard, D Bordereaux, L Thirouard, A Hammoutene, A Montagne, F Dingli, D Loew and 13 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

23 authors.

T Becquard *Université Paris Cité, NF-κB, Differentiation and Cancer, Paris, France.
C Benatar *Université Paris Cité, NF-κB, Differentiation and Cancer, Paris, France.
C BretotUniversité Paris Cité, NF-κB, Differentiation and Cancer, Paris, France.
B EluardUniversité Paris Cité, NF-κB, Differentiation and Cancer, Paris, France.ORCID http://orcid.org/0000-0003-0791-1547
D BordereauxUniversité Paris Cité, NF-κB, Differentiation and Cancer, Paris, France.
L ThirouardNantes Université, Inserm, CNRS, Université d'Angers, Nantes, France.
A HammouteneUniversité Paris Cité, AP-HP. Nord, Department of Pathology, INSERM UMR 1149, FHU MOSAIC, SIRIC InsiTu, Beaujon Hospital, Clichy, France.ORCID http://orcid.org/0000-0001-6928-7431
A MontagneUniversité Paris Cité, NF-κB, Differentiation and Cancer, Paris, France.
F DingliInstitut Curie, PSL Research University, CurieCoreTech Mass Spectrometry Proteomics, Paris, France.ORCID http://orcid.org/0000-0002-7715-2446
D LoewInstitut Curie, PSL Research University, CurieCoreTech Mass Spectrometry Proteomics, Paris, France.ORCID http://orcid.org/0000-0002-9111-8842
C RansyUniversité Paris Cité, CNRS, Inserm, Institut Cochin, Paris, France.
M-C Alves-GuerraUniversité Paris Cité, CNRS, Inserm, Institut Cochin, Paris, France.ORCID http://orcid.org/0000-0002-7918-1216
C CaradeucUniversité Paris Cité, UMR 8601 CNRS, Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques LCBPT, Paris, France.
N CagnardBio-informatic Platform, Université Paris Cité, INSERM US24/CNRS, Unité Mixte de Service (UMS) 3633, Paris, France.ORCID http://orcid.org/0000-0002-9051-1896
M BoissanSorbonne Université, INSERM UMR_S 938, Centre de Recherche Saint-Antoine CRSA, Paris, France.ORCID http://orcid.org/0000-0001-6494-5722
N GiraudUniversité Paris Cité, UMR 8601 CNRS, Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques LCBPT, Paris, France.
F BouillaudUniversité Paris Cité, CNRS, Inserm, Institut Cochin, Paris, France.
G BerthoUniversité Paris Cité, UMR 8601 CNRS, Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques LCBPT, Paris, France.ORCID http://orcid.org/0000-0002-4929-763X
V ParadisUniversité Paris Cité, AP-HP. Nord, Department of Pathology, INSERM UMR 1149, FHU MOSAIC, SIRIC InsiTu, Beaujon Hospital, Clichy, France.ORCID http://orcid.org/0000-0003-3142-3762
D ChironNantes Université, Inserm, CNRS, Université d'Angers, Nantes, France.ORCID http://orcid.org/0000-0002-2199-752X
R DentinUniversité Paris Cité, CNRS, Inserm, Institut Cochin, Paris, France.
C Prip-BuusUniversité Paris Cité, CNRS, Inserm, Institut Cochin, Paris, France.
V BaudUniversité Paris Cité, NF-κB, Differentiation and Cancer, Paris, France. veronique.baud@inserm.fr.ORCID http://orcid.org/0000-0002-4090-718X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells reprogram their metabolism to fulfill their high energetic demand. Lipid metabolism is most often reprogrammed for cancer cell survival and tumor development. The role of alternative oncogenic NF-κB/RelB subunit in the reprogramming of lipid metabolism in cancer is unknown. Here we report that RelB plays a central role at the crossroads of lipid storage and liberation of fatty acids from the lipid droplets to feed the fatty acid oxidation (FAO) and mitochondrial energetic metabolism. High RelB expression defines a subset of hepatocellular carcinoma (HCC) patients and cell lines with a peculiar gene expression profile enriched in lipid catabolic-related genes, including lipases. Functional studies revealed that high RelB activation controls the expression of major lipolytic lipases, including adipose triglyceride lipase (ATGL) and monoglyceride lipase (MAGL), and impacts on HCC cell survival, migration, and tumor development in vivo. Altogether, we uncovered that RelB is a central regulator of the lipid metabolism plasticity and an energy homeostasis sensor in cancer cells.

Indexed as

CarcinogenesisCarcinoma, HepatocellularLipid MetabolismLiver NeoplasmsTranscription Factor RelBAcyltransferasesAnimalsCell Line, TumorCell MovementEnergy MetabolismFatty AcidsGene Expression Regulation, NeoplasticHumansLipaseMetabolic ReprogrammingMiceAcyltransferasesFatty AcidsLipaseRELB protein, humanTranscription Factor RelB

Identifiers

PMID42401573
PMCPMC13612402

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.