Evidence map›Paper›PMID 26028029›Full record

ArticleOncogene2016

Prostate-specific G-protein-coupled receptor collaborates with loss of PTEN to promote prostate cancer progression.

M Rodriguez, S Siwko, L Zeng, J Li, Z Yi, M Liu

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  5. TRAF4-mediated nonproteolytic ubiquitination of androgen receptor promotes castration-resistant prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  6. Review
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  10. The macrophage odorant receptor Olfr78 mediates the lactate-induced M2 phenotype of tumor-associated macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  11. Review
  12. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

M RodriguezCenter for Cancer and Stem Cell Biology, Department of Cellular and Molecular Medicine, Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, TX, USA.
S SiwkoCenter for Cancer and Stem Cell Biology, Department of Cellular and Molecular Medicine, Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, TX, USA.
L ZengCenter for Cancer and Stem Cell Biology, Department of Cellular and Molecular Medicine, Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, TX, USA.
J LiShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
Z YiShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
M LiuCenter for Cancer and Stem Cell Biology, Department of Cellular and Molecular Medicine, Institute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, TX, USA.
Texas A&M University · USEast China Normal University · CN

Funding

Targeting the prostate-specific G-protein coupled receptors in prostate tumorR01CA134731 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI LIU, MINGYAO · 2010 to 2014
$1.5M
NCI NIH HHS 5R01CA134731NCI NIH HHS R01 CA134731
6 · The paper itself

Abstract

Among frequent events in prostate cancer are loss of the tumor-suppressor phosphatase and tensin homologue (PTEN) and overexpression of prostate-specific G-protein-coupled receptor (PSGR), but the potential tumorigenic synergy between these lesions is unknown. Here, we report a new mouse model (PSGR-Pten(Δ/Δ)) combining prostate-specific loss of Pten with probasin promoter-driven PSGR overexpression. By 12 months PSGR-Pten(Δ/Δ) mice developed invasive prostate tumors featuring Akt activation and extensive inflammatory cell infiltration. PSGR-Pten(Δ/Δ) tumors exhibited E-cadherin loss and increased stromal androgen receptor (AR) expression. PSGR overexpression increased LNCaP proliferation, whereas PSGR short hairpin RNA knockdown inhibited proliferation and migration. In conclusion, we demonstrate that PSGR overexpression synergizes with loss of PTEN to accelerate prostate cancer development, and present a novel bigenic mouse model that mimics the human condition, where both PSGR overexpression and loss of PTEN occur concordantly in the majority of advanced prostate cancers, yielding an environment more relevant to studying human prostate cancer.

Indexed as

AnimalsCadherinsCarcinogenesisCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMaleMiceNeoplasm ProteinsProstatic NeoplasmsPTEN PhosphohydrolaseReceptors, OdorantXenograft Model Antitumor AssaysCadherinsNeoplasm ProteinsOR51E2 protein, humanPTEN PhosphohydrolasePTEN protein, humanReceptors, Odorant

Identifiers

PMID26028029
PMCPMC4683109
OpenAlexW1602913332

What OpenQuestion holds

Textmetadata
LicenceTDM
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.