Evidence map›Paper›PMID 23604126›Full record

ArticleOncogene2014

The role of DAB2IP in androgen receptor activation during prostate cancer progression.

K Wu, J Liu, S-F Tseng, C Gore, Z Ning, N Sharifi, L Fazli, M Gleave, P Kapur, G Xiao and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Association of rs3787016 in Long Non-coding RNAsIranian journal of public health · 2018
    Review
  12. Epigenetic Regulation in Prostate Cancer Progression.Current molecular biology reports · 2018
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. DAB2IP in cancer.Oncotarget · 2016
    Review
  19. Article
  20. 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

20 authors at 8 institutions in 4 countries.

K Wu1] Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX, USA [2] Department of Urology, The First Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
J LiuDepartment of Radiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
S-F TsengDepartment of Bioengineering, University of Texas at Arlington, Arlington, TX, USA.
C GoreDepartment of Urology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Z NingDepartment of Urology, The First Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
N SharifiDivision of Hematology/Oncology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
L FazliVancouver Prostate Center, University of British Columbia, Vancouver, British Columbia, Canada.
M GleaveVancouver Prostate Center, University of British Columbia, Vancouver, British Columbia, Canada.
P KapurDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
G XiaoDepartment of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX, USA.
X SunDepartment of Radiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
O K OzDepartment of Radiology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
W MinInterdepartmental Program in Vascular Biology and Transplantation and Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
G AlexandrakisDepartment of Bioengineering, University of Texas at Arlington, Arlington, TX, USA.
C-R YangDepartment of Urology, China Medical University Hospital, Taichung, Taiwan.
C-L Hsieh1] Graduate Institute of Cancer Biology, China Medical University Hospital, Taichung, Taiwan [2] Center for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan [3] Department of Biotechnology, Asia University, Taichung, Taiwan.
H-C Wu1] Department of Urology, China Medical University Hospital, Taichung, Taiwan [2] School of Medicine, China Medical University, Taichung, Taiwan.
D HeDepartment of Urology, The First Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
D XieDepartment of General Surgery, Tongji Cancer Research Institute, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei, China.
J-T Hsieh1] Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX, USA [2] Graduate Institute of Cancer Biology, China Medical University Hospital, Taichung, Taiwan.
The University of Texas Southwestern Medical Center · USChina Medical University · TWChina Medical University Hospital · TWFirst Affiliated Hospital of Xi'an Jiaotong University · CNThe University of Texas at Arlington · USUniversity of British Columbia · CAHuazhong University of Science and Technology · CNYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered androgen-receptor (AR) expression and/or constitutively active AR are commonly associated with prostate cancer (PCa) progression. Targeting AR remains a focal point for designing new strategy of PCa therapy. Here, we have shown that DAB2IP, a novel tumor suppressor in PCa, can inhibit AR-mediated cell growth and gene activation in PCa cells via distinct mechanisms. DAB2IP inhibits the genomic pathway by preventing AR nuclear translocation or phosphorylation and suppresses the non-genomic pathway via its unique functional domain to inactivate c-Src. Also, DAB2IP is capable of suppressing AR activation in an androgen-independent manner. In addition, DAB2IP can inhibit several AR splice variants showing constitutive activity in PCa cells. In DAB2IP(-/-) mice, the prostate gland exhibits hyperplastic epithelia, in which AR becomes more active. Consistently, DAB2IP expression inversely correlates with AR activation status particularly in recurrent or metastatic PCa patients. Taken together, DAB2IP is a unique intrinsic AR modulator in normal cells, and likely can be further developed into a therapeutic agent for PCa.

Indexed as

AnimalsCell Line, TumorDisease ProgressionGene Knockdown TechniquesHumansMaleMiceMice, KnockoutProstatic Neoplasmsras GTPase-Activating ProteinsReceptors, AndrogenReverse Transcriptase Polymerase Chain ReactionTransfectionDAB2IP protein, humanDab2ip protein, mouseras GTPase-Activating ProteinsReceptors, Androgen

Identifiers

PMID23604126
OpenAlexW2093199757

What OpenQuestion holds

Textmetadata
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.