Evidence map›Paper›PMID 28481873›Full record

ArticleOncogene2017

Restoring PU.1 induces apoptosis and modulates viral transactivation via interferon-stimulated genes in primary effusion lymphoma.

H Goto, R Kariya, E Kudo, Y Okuno, K Ueda, H Katano, S Okada

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
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  4. Article
  5. Pioneer factors in viral infection.Frontiers in immunology · 2023
    Review
  6. Article
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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

7 authors at 3 institutions in 1 country.

H GotoDivision of Hematopoiesis, Center for AIDS Research, Kumamoto University, Honjo, Kumamoto, Japan.
R KariyaDivision of Hematopoiesis, Center for AIDS Research, Kumamoto University, Honjo, Kumamoto, Japan.
E KudoDivision of Hematopoiesis, Center for AIDS Research, Kumamoto University, Honjo, Kumamoto, Japan.
Y OkunoDepartments of Hematology, Rheumatology, and Infectious Disease, Kumamoto University Graduate School of Medicine, Honjo, Kumamoto, Japan.
K UedaDivision of Virology, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
H KatanoDepartment of Pathology, National Institute of Infectious Diseases, Toyama, Shinjuku, Tokyo, Japan.
S OkadaDivision of Hematopoiesis, Center for AIDS Research, Kumamoto University, Honjo, Kumamoto, Japan.ORCID 0000-0003-3124-5206
Kumamoto University · JPNational Institute of Infectious Diseases · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary effusion lymphoma (PEL), which is an aggressive subgroup of B-cell lymphoma associated with Kaposi sarcoma-associated herpes virus/human herpes virus-8, is refractory to the standard treatment, and exhibits a poor survival. Although PU.1 is downregulated in PEL, the potential role of its reduction remains to be elucidated. In this investigation, we analyzed the DNA methylation of PU.1 cis-regulatory elements in PEL and the effect of restoring PU.1 on PEL cells. The mRNA level of PU.1 was downregulated in PEL cells. The methylated promoter and enhancer regions of the PU.1 gene were detected in PEL cells. Suppression of cell growth and apoptosis were caused by the restoration of PU.1 in PEL cells. A microarray analysis revealed that interferon-stimulated genes (ISGs) including pro-apoptotic ISGs were strongly increased in BCBL-1 cells after the induction of PU.1. Reporter assays showed that PU.1 transactivated pro-apoptotic ISG promoters, such as the XAF1, OAS1 and TRAIL promoters. Mutations at the PU.1 binding sequences suppressed its transactivation. We confirmed the binding of PU.1 to the XAF1, OAS1 and TRAIL promoters in a chromatin immunoprecipitation assay. PU.1 suppressed ORF57 activation by inducing IRF7. The reinduction of PU.1 reduced formation of ascites and lymphoma cell infiltration of distant organs in PEL xenograft model mice. Collectively, PU.1 has a role in tumor suppression in PEL and its down-regulation is associated with PEL development. Restoring PU.1 with demethylation agents may be a novel therapeutic approach for PEL.

Indexed as

AnimalsApoptosisCell Line, TumorCell ProliferationDNA MethylationHeterograftsHumansInterferon Regulatory Factor-7InterferonsLymphoma, Primary EffusionMaleMiceMice, Inbred NODMicroarray AnalysisPromoter Regions, GeneticProto-Oncogene ProteinsInterferon Regulatory Factor-7InterferonsIRF7 protein, humanProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-Activators

Identifiers

PMID28481873
OpenAlexW2613744689

What OpenQuestion holds

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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.