Evidence map›Paper›PMID 29706654›Full record

ArticleOncogene2018

The essential role of WD repeat domain 77 in prostate tumor initiation induced by Pten loss.

Deon O'Bryant, Zhengxin Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. The Role of WDR77 in Cancer: More than a PRMT5 Interactor.Molecular cancer research : MCR · 2025
    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

2 authors at 2 institutions in 1 country.

Deon O'BryantDepartment of Biological Sciences, The Center for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, GA, 30314, USA.
Zhengxin WangDepartment of Biological Sciences, The Center for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, GA, 30314, USA. zwang@cau.edu.
Center for Cancer Research · USClark Atlanta University · US

Funding

NIH HHS 5G12MD007590NIH HHS 5P20MD002285NIH HHS R25GM06414
6 · The paper itself

Abstract

Prostate cancer is the most commonly diagnosed malignancy among men, but few genetic factors that drive prostate cancer initiation have been identified. The WD repeat domain 77 (Wdr77) protein is essential for cellular proliferation when localizes in the cytoplasm of epithelial cells at the early stage of prostate development. In the adult prostate, it is transported into the nucleus and functions as a co-regulator of the androgen receptor to promote cellular differentiation and prostate function. This developmental process is reversed during prostate tumorigenesis, i.e., Wdr77 is translocated from the nucleus into the cytoplasm to drive proliferation of prostate cancer cells. In this study, we used in vivo genetic studies to further investigate the role of Wdr77 in prostate tumorigenesis. We found that prostate-specific deletion of Wdr77 abolished prostate tumor initiation induced by loss of the tumor suppressor Pten. Mechanistically, Wdr77 ablation inhibited E2F3 activation and enhanced TGFβ signaling, leading to attenuated cellular proliferation induced by loss of Pten. These findings establish a critical role of Wdr77 for prostate tumor initiation.

Indexed as

AnimalsCarcinogenesisCell DifferentiationCell Line, TumorCell NucleusCell ProliferationCytoplasmEpithelial CellsMaleMiceProstateProstatic NeoplasmsPTEN PhosphohydrolaseReceptors, AndrogenSignal TransductionTranscription FactorsPTEN PhosphohydrolasePten protein, mouseReceptors, AndrogenTranscription FactorsTransforming Growth Factor betaWDR77 protein, mouse

Identifiers

PMID29706654
OpenAlexW2801261142

What OpenQuestion holds

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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.