Evidence map›Paper›PMID 26790128›Full record

ArticleCancer science2016

Downregulation of WDR20 due to loss of 14q is involved in the malignant transformation of clear cell renal cell carcinoma.

Mika Takahashi, Yoshiyuki Tsukamoto, Tomoki Kai, Akinori Tokunaga, Chisato Nakada, Naoki Hijiya, Tomohisa Uchida, Tsutomu Daa, Takeo Nomura, Fuminori Sato and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. WDR20 prevents hepatocellular carcinoma senescence by orchestrating the simultaneous USP12/46-mediated deubiquitination of c-Myc.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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

13 authors at 1 institution in 1 country.

Mika TakahashiDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Yoshiyuki TsukamotoDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Tomoki KaiDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Akinori TokunagaResearch Promotion Institute, Faculty of Medicine, Oita University, Oita, Japan.
Chisato NakadaDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Naoki HijiyaDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Tomohisa UchidaDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Tsutomu DaaDepartment of Diagnostic Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Takeo NomuraDepartment of Urology, Faculty of Medicine, Oita University, Oita, Japan.
Fuminori SatoDepartment of Urology, Faculty of Medicine, Oita University, Oita, Japan.
Hiromitsu MimataDepartment of Urology, Faculty of Medicine, Oita University, Oita, Japan.
Keiko MatsuuraDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Masatsugu MoriyamaDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Oita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously, we reported that genomic loss of 14q occurs more frequently in high-grade than in low-grade clear cell renal cell carcinomas (ccRCCs), and has a significant impact on the levels of expression of genes located in this region, suggesting that such genes may be involved in the malignant transformation of ccRCCs. Here, we found that six of the genes located in the minimal common region of 14q loss were significantly downregulated in high-grade ccRCCs due to copy number loss. Using a dataset from The Cancer Genome Atlas Research Network, we found that downregulation of one of these six genes, WDR20, was significantly associated with poorer outcome in patients with ccRCC, suggesting that WDR20 downregulation may be involved in the malignant transformation of ccRCCs. In functional assays, exogenous WDR20 significantly inhibited the growth of RCC cell lines and induced apoptosis. Interestingly, the phosphorylation levels of ERK and protein kinase B/AKT, which reportedly contribute to the malignant phenotype of RCC cells, were clearly reduced by exogenous expression of WDR20. Thus, our data suggest that downregulation of WDR20 due to 14q loss may be involved in the malignant transformation of ccRCCs, in part through activation of the ERK and protein kinase B/AKT pathways.

Indexed as

ApoptosisCarcinoma, Renal CellCarrier ProteinsCell ProliferationCell Transformation, NeoplasticChromosomes, Human, Pair 14Gene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemOncogene Protein v-aktCarrier ProteinsOncogene Protein v-aktWDR20 protein, human14q lossApoptosisclear cell renal cell carcinomaThe Cancer Genome AtlasWDR20

Identifiers

PMID26790128
PMCPMC4832870
OpenAlexW2282648889

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.