Evidence map›Paper›PMID 23770850›Full record

ArticleOncogene2014

Coordinated regulation of the immunoproteasome subunits by PML/RARα and PU.1 in acute promyelocytic leukemia.

X-W Yang, P Wang, J-Q Liu, H Zhang, W-D Xi, X-H Jia, K-K Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  5. Article
  6. Article
  7. Review
  8. Proteasome: Role in T Cell Function Regulation.International journal of biological sciences · 2025
    Review
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  11. 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.

X-W YangState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China.
P WangState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China.
J-Q LiuState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China.
H ZhangState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China.
W-D XiState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China.
X-H JiaState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China.
K-K WangState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China.
Shanghai Institute of Hematology · CNShanghai Jiao Tong University · CNRuijin Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recognition and elimination of malignant cells by cytotoxic T lymphocytes depends on antigenic peptides generated by proteasomes. It has been established that impairment of the immunoproteasome subunits, that is, PSMB8, PSMB9 and PSMB10 (PSMBs), is critical for malignant cells to escape immune recognition. We report here the regulatory mechanism of the repression of PU.1-dependent activation of PSMBs by PML/RARα in the pathogenesis of acute promyelocytic leukemia (APL) and the unidentified function of all-trans retinoic acid (ATRA) as an immunomodulator in the treatment of APL. Chromatin immunoprecipitation and luciferase reporter assays showed that PU.1 directly bound to and coordinately transactivated the promoters of PSMBs, indicating that PSMBs were transcriptional targets of PU.1 and PU.1 regulated their basal expression. Analysis of expression profiling data from a large population of acute myeloid leukemia (AML) patients revealed that the expression levels of PSMBs were significantly lower in APL patients than in non-APL AML patients. Further evidence demonstrated that the decrease in their expression was achieved through PML/RARα-mediated repression of both PU.1-dependent transactivation and PU.1 expression. Moreover, ATRA but not arsenic trioxide induced the expression of PSMBs in APL cells, indicating that ATRA treatment might activate the antigen-processing/presentation machinery. Finally, the above observations were confirmed in primary APL samples. Collectively, our data demonstrate that PML/RARα suppresses PU.1-dependent activation of the immunosubunits, which may facilitate the escape of APL cells from immune surveillance in leukemia development, and ATRA treatment is able to reactivate their expression, which would promote more efficient T-cell-mediated recognition in the treatment.

Indexed as

Gene Expression Regulation, LeukemicAntigen PresentationArsenicalsArsenic TrioxideCysteine EndopeptidasesGene Expression Regulation, EnzymologicHL-60 CellsHumansImmunologic FactorsLeukemia, Promyelocytic, AcuteNuclear ProteinsOxidesPromoter Regions, GeneticPromyelocytic Leukemia ProteinProteasome Endopeptidase ComplexProtein BindingArsenicalsArsenic TrioxideCysteine EndopeptidasesImmunologic FactorsLMP-2 proteinLMP7 proteinNuclear ProteinsOxidesPML protein, humanPromyelocytic Leukemia ProteinProteasome Endopeptidase ComplexProtein SubunitsProto-Oncogene ProteinsProto-Oncogene Protein Spi-1PSMB10 protein, humanRARA protein, humanReceptors, Retinoic AcidRetinoic Acid Receptor alphaTrans-ActivatorsTranscription FactorsTretinoinTumor Suppressor Proteins

Identifiers

PMID23770850
OpenAlexW2091005907

What OpenQuestion holds

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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.