Evidence map›Paper›PMID 23795761›Full record

ArticleBritish journal of haematology2013

LITAF, a BCL6 target gene, regulates autophagy in mature B-cell lymphomas.

Cristina Bertolo, Sergio Roa, Ainara Sagardoy, Maria Mena-Varas, Eloy F Robles, Jose I Martinez-Ferrandis, Xavier Sagaert, Thomas Tousseyn, Alberto Orta, Izidore S Lossos and 6 more

Abstract read
In one paragraph

Article in British journal of haematology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 3 pooled it
–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

27 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Guideline
  2. Pooled it
  3. Guideline
  4. Article
  5. Article
  6. Circadian clock protein BMAL1 broadly influences autophagy and endolysosomal function in astrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Autophagy and Metabolism in Normal and Malignant Hematopoiesis.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Oncotarget · 2018
    Article
  18. Review
  19. Review
  20. Article
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

16 authors.

Cristina BertoloDivision of Oncology, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain.
Sergio Roa
Ainara Sagardoy
Maria Mena-Varas
Eloy F Robles
Jose I Martinez-Ferrandis
Xavier Sagaert
Thomas Tousseyn
Alberto Orta
Izidore S Lossos
Salomon Amar
Yasodha Natkunam
Javier Briones
Ari Melnick
Raquel Malumbres
Jose A Martinez-Climent

Funding

Role of LITAF in Inflammatory ProcessesR01DE014079 · NIDCR · NEW YORK MEDICAL COLLEGE · PI AMAR, SALOMON · 2002 to 2016
$5.4M
Transcriptional silencing by the BCL6 oncoproteinR01CA104348 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MELNICK, ARI M. · 2004 to 2014
$2.6M
NCI NIH HHS R01 CA104348NIDCR NIH HHS R01 DE014079
6 · The paper itself

Abstract

We have previously reported that LITAF is silenced by promoter hypermethylation in germinal centre-derived B-cell lymphomas, but beyond these data the regulation and function of lipopolysaccharide-induced tumour necrosis factor (TNF) factor (LITAF) in B cells are unknown. Gene expression and immunohistochemical studies revealed that LITAF and BCL6 show opposite expression in tonsil B-cell subpopulations and B-cell lymphomas, suggesting that BCL6 may regulate LITAF expression. Accordingly, BCL6 silencing increased LITAF expression, and chromatin immunoprecipitation and luciferase reporter assays demonstrated a direct transcriptional repression of LITAF by BCL6. Gain- and loss-of-function experiments in different B-cell lymphoma cell lines revealed that, in contrast to its function in monocytes, LITAF does not induce lipopolysaccharide-mediated TNF secretion in B cells. However, gene expression microarrays defined a LITAF-related transcriptional signature containing genes regulating autophagy, including MAP1LC3B (LC3B). In addition, immunofluorescence analysis co-localized LITAF with autophagosomes, further suggesting a possible role in autophagy modulation. Accordingly, ectopic LITAF expression in B-cell lymphoma cells enhanced autophagy responses to starvation, which were impaired upon LITAF silencing. Our results indicate that the BCL6-mediated transcriptional repression of LITAF may inhibit autophagy in B cells during the germinal centre reaction, and suggest that the constitutive repression of autophagy responses in BCL6-driven lymphomas may contribute to lymphomagenesis.

Indexed as

AutophagyB-Lymphocyte SubsetsCell Line, TumorDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansIntronsLymphoma, B-CellNeoplasm ProteinsNuclear ProteinsProto-Oncogene Proteins c-bcl-6Transcription FactorsTranscription, GeneticTumor Necrosis Factor-alphaBCL6 protein, humanDNA-Binding ProteinsLITAF protein, humanNeoplasm ProteinsNuclear ProteinsProto-Oncogene Proteins c-bcl-6Transcription FactorsTumor Necrosis Factor-alphaautophagyB cellsgerminal centreNon-hodgkin lymphomatranscription factors

Identifiers

PMID23795761
PMCPMC4111142

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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.