Evidence map›Paper›PMID 16449965›Full record

ArticleOncogene2006

Regulator of G-protein signaling 2 (RGS2) inhibits androgen-independent activation of androgen receptor in prostate cancer cells.

X Cao, J Qin, Y Xie, O Khan, F Dowd, M Scofield, M-F Lin, Y Tu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.3field-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

55 citing papers in PubMed, 96 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. The C/C Genotype of rs1231760 inDiagnostics (Basel, Switzerland) · 2024
    Article
  5. Review
  6. Review
  7. Review
  8. Polyphenon E Effects on Gene Expression in PC-3 Prostate Cancer Cells.International journal of molecular sciences · 2022
    Article
  9. Article
  10. Effect of the regulator of G-protein signaling 2 on the proliferation and invasion of oral squamous cell carcinoma cells and its molecular mechanism.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2021
    Article
  11. Article
  12. Article
  13. miR-183-5p Aggravates Breast Cancer Development via Mediation of RGS2.Computational and mathematical methods in medicine · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

8 authors at 2 institutions in 1 country.

X CaoDepartment of Pharmacology, Creighton University School of Medicine, Omaha, NE 68178, USA.
J Qin
Y Xie
O Khan
F Dowd
M Scofield
M-F Lin
Y Tu
Creighton University · USUniversity of Nebraska Medical Center · US

Funding

SUPPRESSIVE ROLE OF TGFBETA IN METASTASIS OF COLON CANCERP20RR018759 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JOHNSON, KEITH R · 2003 to 2011
$17.9M
SIGNALING IN ANDROGEN REFRACTORY PROSTATE CANCERR01CA088184 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI LIN, MING-FONG · 2000 to 2010
$2.6M
NCI NIH HHS CA88184NCRR NIH HHS P20 RR018759
6 · The paper itself

Abstract

Hormones acting through G protein-coupled receptors (GPCRs) can cause androgen-independent activation of androgen receptor (AR) in prostate cancer cells. Regulators of G-protein signaling (RGS) proteins, through their GTPase activating protein (GAP) activities, inhibit GPCR-mediated signaling by inactivating G proteins. Here, we identified RGS2 as a gene specifically downregulated in androgen-independent prostate cancer cells. Expression of RGS2, but not other RGS proteins, abolished androgen-independent AR activity in androgen-independent LNCaP cells and CWR22Rv1 cells. In LNCaP cells, RGS2 inhibited G(q)-coupled GPCR signaling. Expression of exogenous wild-type RGS2, but not its GAP-deficient mutant, significantly reduced AR activation by constitutively activated G(q)Q209L mutant whereas silencing endogenous RGS2 by siRNA enhanced G(q)Q209L-stimulated AR activity. RGS2 had no effect on RGS-insensitive G(q)Q209L/G188S-induced AR activation. Furthermore, extracellular signal-regulated kinase 1/2 (ERK1/2) was found to be involved in RGS2-mediated regulation of androgen-independent AR activity. In addition, RGS2 functioned as a growth suppressor for androgen-independent LNCaP cells whereas androgen-sensitive LNCaP cells with RGS2 silencing had a growth advantage under steroid-reduced conditions. Finally, RGS2 expression level was significantly decreased in human prostate tumor specimens. Taken together, our results suggest RGS2 as a novel regulator of AR signaling and its repression may be an important step during prostate tumorigenesis and progression.

Indexed as

AdenocarcinomaAndrogensDown-RegulationGene Expression Regulation, NeoplasticHumansMaleMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MutationProstatic NeoplasmsReceptors, AndrogenRGS ProteinsRNA, Small InterferingTumor Cells, CulturedAndrogensMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Receptors, AndrogenRGS2 protein, humanRGS ProteinsRNA, Small Interfering

Identifiers

PMID16449965
OpenAlexW2059521326

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.