Evidence map›Paper›PMID 18451148›Full record

ArticleCancer research2008

Androgens transduce the G alphas-mediated activation of protein kinase A in prostate cells.

Gargi Bagchi, Juanjuan Wu, John French, Jae Kim, Nader H Moniri, Yehia Daaka

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. The importance of protein kinase A in prostate cancer: relationship to patient outcome in Radiation Therapy Oncology Group trial 92-02.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Role of androgens in cardiovascular pathology.Vascular health and risk management · 2018
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Identification of betaArrestin2 as a corepressor of androgen receptor signaling in prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  16. Article
  17. 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

6 authors at 2 institutions in 2 countries.

Gargi BagchiDepartment of Pathology, Medical College of Georgia, Augusta, GA 30912, USA.
Juanjuan Wu
John French
Jae Kim
Nader H Moniri
Yehia Daaka
Augusta University · USIstituto Superiore di Sanità · IT

Funding

G Protein-Dependent Growth of Prostate CancerR01AG017952 · NIA · DUKE UNIVERSITY · PI DAAKA, YEHIA · 2001 to 2004
$924k
Dissecting the role of G proteins in prostate cancerR01DK060917 · NIDDK · DUKE UNIVERSITY · PI DAAKA, YEHIA · 2001 to 2004
$921k
NIA NIH HHS AG17952NIA NIH HHS R01 AG017952NIDDK NIH HHS DK60917NIDDK NIH HHS R01 DK060917
6 · The paper itself

Abstract

Androgens regulate the development and function of male reproductive organs and play a crucial role in the onset and progression of prostate cancer. Androgen action is primarily mediated through the nuclear androgen receptor (AR) which acts as a ligand-dependent transcription factor. This mode of androgen action takes hours to manifest and is called the genomic pathway. The androgen-mediated genomic responses require activity of cyclic AMP (cAMP)-dependent protein kinase (PKA). Androgens also act through nongenomic pathways in certain cell types to evoke rapid responses (manifested in minutes) that are mediated through changes in ion currents and second messengers. Here, we show that androgen causes the rapid and cAMP-dependent activation of PKA in prostate cells. The androgen-induced PKA activation is not inhibited by nuclear AR antagonist bicalutamide and can be observed in cells that do not express nuclear AR gene. Reduction of G alphas expression with siRNA attenuates the androgen-mediated activation of PKA, which is required for the androgen-induced prostate cell proliferation. We conclude that androgen actively evokes a nongenomic signaling pathway to activate PKA that is needed for the genomic functioning of nuclear AR. The inhibition of PKA activation, together with standard AR-targeted therapies, may be more efficacious for treatment of patients with prostate cancer.

Indexed as

AndrogensAnimalsCell NucleusCells, CulturedCyclic AMPCyclic AMP-Dependent Protein KinasesEnzyme ActivationEpithelial CellsGTP-Binding Protein alpha Subunits, GsHumansMaleMiceModels, BiologicalProstateReceptors, AndrogenAndrogensCyclic AMPCyclic AMP-Dependent Protein KinasesGTP-Binding Protein alpha Subunits, GsReceptors, Androgen

Identifiers

PMID18451148
PMCPMC3861896
OpenAlexW2083234838

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.