Evidence map›Paper›PMID 29686263›Full record

ArticleCell death & disease2018

BAP1 induces cell death via interaction with 14-3-3 in neuroblastoma.

Wondossen Sime, Qiankun Niu, Yasmin Abassi, Katarzyna Chmielarska Masoumi, Reihaneh Zarrizi, Julie Bonne Køhler, Sven Kjellström, Vito Alessandro Lasorsa, Mario Capasso, Haian Fu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

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  6. An overview of BAP1 biological functions and current therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2025
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  17. Deubiquitinases: Modulators of Different Types of Regulated Cell Death.International journal of molecular sciences · 2021
    Review
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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

11 authors at 5 institutions in 4 countries.

Wondossen SimeDepartment of Laboratory Medicine, Translational Cancer Research, Lund University, Medicon Village, Lund, Sweden.
Qiankun NiuDepartment of Pharmacology and Emory Chemical Biology Discovery Center, Emory University School of Medicine, Atlanta, USA.
Yasmin AbassiDepartment of Laboratory Medicine, Translational Cancer Research, Lund University, Medicon Village, Lund, Sweden.
Katarzyna Chmielarska MasoumiDepartment of Laboratory Medicine, Translational Cancer Research, Lund University, Medicon Village, Lund, Sweden.
Reihaneh ZarriziDepartment of Laboratory Medicine, Translational Cancer Research, Lund University, Medicon Village, Lund, Sweden.
Julie Bonne KøhlerDepartment of Laboratory Medicine, Translational Cancer Research, Lund University, Medicon Village, Lund, Sweden.
Sven KjellströmDepartment of Clinical Sciences Lund, Neurology, Lund University, Faculty of Medicine, Lund, Sweden.
Vito Alessandro LasorsaUniversità degli Studi di Napoli Federico II, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, via Sergio Pansini 5, 80131, Naples, Italy.
Mario CapassoUniversità degli Studi di Napoli Federico II, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, via Sergio Pansini 5, 80131, Naples, Italy.
Haian FuDepartment of Pharmacology and Emory Chemical Biology Discovery Center, Emory University School of Medicine, Atlanta, USA.
Ramin MassoumiDepartment of Laboratory Medicine, Translational Cancer Research, Lund University, Medicon Village, Lund, Sweden. Ramin.Massoumi@med.lu.se.
Lund University · SEMedicon Village · SEEmory University · USCeinge Biotecnologie Avanzate (Italy) · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BRCA1-associated protein 1 (BAP1) is a nuclear deubiquitinating enzyme that is associated with multiprotein complexes that regulate key cellular pathways, including cell cycle, cellular differentiation, cell death, and the DNA damage response. In this study, we found that the reduced expression of BAP1 pro6motes the survival of neuroblastoma cells, and restoring the levels of BAP1 in these cells facilitated a delay in S and G2/M phase of the cell cycle, as well as cell apoptosis. The mechanism that BAP1 induces cell death is mediated via an interaction with 14-3-3 protein. The association between BAP1 and 14-3-3 protein releases the apoptotic inducer protein Bax from 14-3-3 and promotes cell death through the intrinsic apoptosis pathway. Xenograft studies confirmed that the expression of BAP1 reduces tumor growth and progression in vivo by lowering the levels of pro-survival factors such as Bcl-2, which in turn diminish the survival potential of the tumor cells. Patient data analyses confirmed the finding that the high-BAP1 mRNA expression correlates with a better clinical outcome. In summary, our study uncovers a new mechanism for BAP1 in the regulation of cell apoptosis in neuroblastoma cells.

Indexed as

ApoptosisCell CycleGene Expression Regulation, Neoplastic14-3-3 ProteinsAnimalsbcl-2-Associated X ProteinCell Line, TumorFemaleHumansMiceMice, NudeNeuroblastomaProto-Oncogene Proteins c-bcl-2Tumor Suppressor ProteinsUbiquitin Thiolesterase14-3-3 ProteinsBAP1 protein, humanBAX protein, humanbcl-2-Associated X ProteinBCL2 protein, humanProto-Oncogene Proteins c-bcl-2Tumor Suppressor ProteinsUbiquitin Thiolesterase

Identifiers

PMID29686263
PMCPMC5913307
OpenAlexW2802080867

What OpenQuestion holds

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Registered trials

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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.