Evidence map›Paper›PMID 32034308›Full record

ArticleOncogene2020

Stabilization of β-catenin upon B-cell receptor signaling promotes NF-kB target genes transcription in mantle cell lymphoma.

Gregory Lazarian, Chloe Friedrich, Anne Quinquenel, Julie Tran, Souhail Ouriemmi, Elisabetta Dondi, Antoine Martin, Imane Mihoub, David Chiron, Céline Bellanger and 11 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. 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
1.3field-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, 22 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

21 authors at 7 institutions in 4 countries.

Gregory Lazarian *U978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
Chloe Friedrich *U978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
Anne QuinquenelU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
Julie TranU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
Souhail OuriemmiU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
Elisabetta DondiU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
Antoine MartinU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
Imane MihoubU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
David ChironCentre de Recherches en Cancérologie et Immunologie Nantes-Angers, U1232 INSERM, Centre National de la Recherche Scientifique (CNRS) ERL6001, Université de Nantes, Nantes, France.
Céline BellangerCentre de Recherches en Cancérologie et Immunologie Nantes-Angers, U1232 INSERM, Centre National de la Recherche Scientifique (CNRS) ERL6001, Université de Nantes, Nantes, France.
Carole FleuryU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
Pascal GélébartDepartment of clinical science, University of Bergen, Bergen, Norway.
Emmet McCormackDepartment of clinical science, University of Bergen, Bergen, Norway.
Dominique LedouxU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
Catherine ThieblemontHématologie, Hôpital Saint-Louis, Assistance Publique-Hôpitaux de Paris, Paris, France.
Jacek MarzecDepartment of Clinical Pathology, University of Melbourne, Melbourne, VIC, Australia.
John G GribbenBarts Cancer Institute, Queen Mary University of London, London, UK.
Florence CymbalistaU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
Nadine Varin-BlankU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France. nadine.varin@inserm.fr.
Laura GardanoU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France.
Fanny Baran-MarszakU978 Institut National de la Santé et de la Recherche Médicale, Bobigny, France. fanny.baran-marszak@aphp.fr.ORCID http://orcid.org/0000-0002-3723-2927
Inserm · FRCentre National de la Recherche Scientifique · FRUniversity of Bergen · NOAssistance Publique – Hôpitaux de Paris · FRQueen Mary University of London · GBThe University of Melbourne · AUUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B-cell receptor (BCR) signaling pathways and interactions with the tumor microenvironment account for mantle cell lymphoma (MCL) cells survival in lymphoid organs. In several MCL cases, the WNT/β-catenin canonical pathway is activated and β-catenin accumulates into the nucleus. As both BCR and β-catenin are important mediators of cell survival and interaction with the microenvironment, we investigated the crosstalk between BCR and WNT/β-catenin signaling and analyzed their impact on cellular homeostasis as well as their targeting by specific inhibitors. β-catenin was detected in all leukemic MCL samples and its level of expression rapidly increased upon BCR stimulation. This stabilization was hampered by the BCR-pathway inhibitor Ibrutinib, supporting β-catenin as an effector of the BCR signaling. In parallel, MCL cells as compared with normal B cells expressed elevated levels of WNT16, a NF-κB target gene. Its expression increased further upon BCR stimulation to participate to the stabilization of β-catenin. Upon BCR stimulation, β-catenin translocated into the nucleus but did not induce a Wnt-like transcriptional response, i.e., TCF/LEF dependent. β-catenin rather participated to the regulation of NF-κB transcriptional targets, such as IL6, IL8, and IL1. Oligo pull down and chromatin immunoprecipitation experiments demonstrated that β-catenin is part of a protein complex that binds the NF-κB DNA consensus sequence, strengthening the idea of an association between the two proteins. An inhibitor targeting β-catenin transcriptional interactions hindered both NF-κB DNA recruitment and induced primary MCL cells apoptosis. Thus, β-catenin likely represents another player through which BCR signaling impacts on MCL cell survival.

Indexed as

AnimalsApoptosisbeta CateninB-LymphocytesCell LineCell Line, TumorCell NucleusCell SurvivalFemaleHEK293 CellsHomeostasisHumansLymphoma, Mantle-CellMiceNF-kappa BReceptors, Antigen, B-Cellbeta CateninCTNNB1 protein, humanNF-kappa BReceptors, Antigen, B-CellTCF Transcription Factors

Identifiers

PMID32034308
OpenAlexW3004675143

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.