Evidence map›Paper›PMID 26011428›Full record

ArticleCancer science2015

Functional differences between wild-type and mutant-type BRCA1-associated protein 1 tumor suppressor against malignant mesothelioma cells.

Shuhei Hakiri, Hirotaka Osada, Futoshi Ishiguro, Hideki Murakami, Yuko Murakami-Tonami, Kohei Yokoi, Yoshitaka Sekido

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Phenotype-Specific Recalibration of MAVE Data Enables Repurposing ofmedRxiv : the preprint server for health sciences · 2026
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  14. Malignant pleural mesothelioma: an update.Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia · 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

7 authors at 2 institutions in 1 country.

Shuhei HakiriDivision of Molecular Oncology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Hirotaka OsadaDivision of Molecular Oncology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Futoshi IshiguroDivision of Molecular Oncology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Hideki MurakamiDivision of Molecular Oncology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Yuko Murakami-TonamiDivision of Molecular Oncology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Kohei YokoiDepartment of Thoracic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yoshitaka SekidoDivision of Molecular Oncology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Aichi Cancer Center · JPNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant mesothelioma (MM) shows inactivation of the BRCA1-associated protein 1 (BAP1) gene. In this study, we found BAP1 mutations in 5 (26%) of the 19 cell lines that we established from Japanese MM patients, and examined functional differences between the WT and mutant BAP1. First, we studied the subcellular localization of BAP1, demonstrating that the WT primarily resides in the nucleus and that the mutant BAP1 is found in the cytoplasm of the cells. Transduction of the WT BAP1 vector into MM cells with homozygous deletion at the BAP1 3' side resulted in both inhibition of cell proliferation and anchorage-independent cell growth, whereas BAP1 mutants of a missense or C-terminal truncated form showed impaired growth inhibitory effects. Next, we studied how BAP1 is involved in MM cell survival after irradiation (IR), which causes DNA damage. After IR, we found that both WT and mutant BAP1 were similarly phosphorylated and phospho-BAP1 localized mainly in the nucleus. Interestingly, BRCA1 proteins were decreased in the MM cells with BAP1 deletion, and transduction of the mutants as well as WT BAP1 increased BRCA1 proteins, suggesting that BAP1 may promote DNA repair partly through stabilizing BRCA1. Furthermore, using the MM cells with BAP1 deletion, we found that WT BAP1, and even a missense mutant, conferred a higher survival rate after IR compared to the control vector. Our results suggested that, whereas WT BAP1 suppresses MM cell proliferation and restores cell survival after IR damage, some mutant BAP1 may also moderately retain these functions.

Indexed as

Cell Line, TumorCell ProliferationDNA Mutational AnalysisHumansLung NeoplasmsMesotheliomaMesothelioma, MalignantMutationTumor Suppressor ProteinsUbiquitin ThiolesteraseBAP1 protein, humanTumor Suppressor ProteinsUbiquitin ThiolesteraseBAP1malignant mesotheliomamutationsubcellular localizationtumor suppressor gene

Identifiers

PMID26011428
PMCPMC4556387
OpenAlexW1859240457

What OpenQuestion holds

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LicenceCC BY-NC
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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.