Evidence map›Paper›PMID 25569233›Full record

ArticlePLoS genetics2015

The Tumor Suppressor BCL7B Functions in the Wnt Signaling Pathway.

Tomoko Uehara, Eriko Kage-Nakadai, Sawako Yoshina, Rieko Imae, Shohei Mitani

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. 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
2.3field-weighted citation impact, top 13% 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, 42 citations in OpenAlex.

  1. Structure and molecular function of the BCL7 proteins.Biochemical Society transactions · 2026
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  15. BCL7A as a novel prognostic biomarker for glioma patients.Journal of translational medicine · 2021
    Article
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  17. Genome evolution of blind subterranean mole rats: Adaptive peripatric versus sympatric speciation.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

5 authors at 1 institution in 1 country.

Tomoko UeharaDepartment of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo, Japan.
Eriko Kage-NakadaiDepartment of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo, Japan.
Sawako YoshinaDepartment of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo, Japan.
Rieko ImaeDepartment of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo, Japan.
Shohei MitaniDepartment of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo, Japan; Tokyo Women's Medical University Institute for Integrated Medical Sciences, Tokyo, Japan.
Tokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human BCL7 gene family consists of BCL7A, BCL7B, and BCL7C. A number of clinical studies have reported that BCL7 family is involved in cancer incidence, progression, and development. Among them, BCL7B, located on chromosome 7q11.23, is one of the deleted genes in patients with Williams-Beuren syndrome. Although several studies have suggested that malignant diseases occurring in patients with Williams-Beuren syndrome are associated with aberrations in BCL7B, little is known regarding the function of this gene at the cellular level. In this study, we focused on bcl-7, which is the only homolog of BCL7 gene family in Caenorhabditis elegans, and analyzed bcl-7 deletion mutants. As a result, we found that bcl-7 is required for the asymmetric differentiation of epithelial seam cells, which have self-renewal properties as stem cells and divide asymmetrically through the WNT pathway. Distal tip cell development, which is regulated by the WNT pathway in Caenorhabditis elegans, was also affected in bcl-7-knockout mutants. Interestingly, bcl-7 mutants exhibited nuclear enlargement, reminiscent of the anaplastic features of malignant cells. Furthermore, in KATOIII human gastric cancer cells, BCL7B knockdown induced nuclear enlargement, promoted the multinuclei phenotype and suppressed cell death. In addition, this study showed that BCL7B negatively regulates the Wnt-signaling pathway and positively regulates the apoptotic pathway. Taken together, our data indicate that BCL7B/BCL-7 has some roles in maintaining the structure of nuclei and is involved in the modulation of multiple pathways, including Wnt and apoptosis. This study may implicate a risk of malignancies with BCL7B-deficiency, such as Williams-Beuren syndrome.

Indexed as

AnimalsApoptosisCaenorhabditis elegansCell DifferentiationCell NucleusEpithelial CellsGenes, Tumor SuppressorHumansNeoplasmsPhenotypeProteinsSequence DeletionStem CellsWilliams SyndromeWnt Signaling PathwayBCL7B protein, humanProteins

Identifiers

PMID25569233
PMCPMC4287490
OpenAlexW2070430772

What OpenQuestion holds

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LicenceCC BY
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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.