Evidence map›Paper›PMID 19274665›Full record

ArticleThe Prostate2009

Soluble factors derived from stroma activated androgen receptor phosphorylation in human prostate LNCaP cells: roles of ERK/MAP kinase.

Katsumi Shigemura, Shuji Isotani, Ruoxiang Wang, Masato Fujisawa, Akinobu Gotoh, Fray F Marshall, Haiyen E Zhau, Leland W K Chung

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Fibroblasts prolong serum prostate-specific antigen decline after androgen deprivation therapy in prostate cancer.Laboratory investigation; a journal of technical methods and pathology · 2016
    Article
  8. Article
  9. Article
  10. Proline-Directed Androgen Receptor Phosphorylation.Journal of molecular and genetic medicine : an international journal of biomedical research · 2013
    Article
  11. Article
  12. Article
  13. Mini-review: androgen receptor phosphorylation in prostate cancer.American journal of clinical and experimental urology · 2013
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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 3 institutions in 2 countries.

Katsumi ShigemuraMolecular Urology and Therapeutics Program, Department of Urology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Shuji Isotani
Ruoxiang Wang
Masato Fujisawa
Akinobu Gotoh
Fray F Marshall
Haiyen E Zhau
Leland W K Chung
Emory University · USHyogo Medical University · JPKobe University · JP

Funding

Prostate Cancer Bone Metastasis: Biology and TargetingP01CA098912 · NCI · EMORY UNIVERSITY · PI ZAYZAFOON, MAJD · 2003 to 2019
$24.0M
Tissue and Animal UseU54CA119338 · NCI · EMORY UNIVERSITY · PI WANG, DONGMEI · 2005 to 2009
$18.4M
Nanotechnology Linking Biomarkers with Cancer BehaviorR01CA108468 · NCI · EMORY UNIVERSITY · PI NIE, SHUMING · 2004 to 2008
$6.9M
Beta 2-Microglobulin signaling and targeting in bone metastasisR01CA122602 · NCI · CEDARS-SINAI MEDICAL CENTER · PI CHUNG, LELAND W.K. · 2009 to 2013
$1.5M
NCI NIH HHS P01 CA098912NCI NIH HHS R01 CA108468NCI NIH HHS R01 CA122602NCI NIH HHS U54 CA119338
6 · The paper itself

Abstract

backgroundAccumulated evidence suggests stromal-epithelial interactions are critical to the progression of prostate cancer. In this study, we characterized AR phosphorylation in LNCaP cells co-cultured with the conditioned medium (CM) from human prostate stromal fibroblasts.

methodsCM harvested from prostate stromal fibroblasts was added to LNCaP cells, and both anchorage-dependent and -independent growth was determined. Status of AR phosphorylation at Ser-81 and Ser-213 was assessed by immunoblot analysis. ERK kinase activity was measured using MBP-2 protein as the substrate.

resultsThe growth of LNCaP cells on plastic dishes increased by 1.7-fold upon exposure to stromal CM or androgen, and their combination resulted in additive growth (2.4-fold). Anchorage-independent growth of LNCaP cells in soft agar, however, was induced synergistically at 80-fold by both stromal CM and androgen. Stromal CM or androgen alone induced LNCaP cell growth by 10- and 26-fold, respectively. We observed ERK kinase inhibitor, U0126, but not phosphatidylinositol 3-kinase (PI-3K), LY294002, or protein kinase A (PKA) inhibitor, H-89, inhibited stromal CM or androgen-induced PSA promoter luciferase activities, and anchorage-independent growth of LNCaP cells. Our results demonstrated for the first time how stromal CM acts in synergy with androgen by activation of ERK kinase and AR phosphorylation at Ser-81 but not Ser-213, for AR-regulated PSA promoter and anchorage-independent growth of human prostate cancer cells.

conclusionsA stromal factor-activated ERK pathway mediated by AR phosphorylation at Ser-81 could be responsible for stimulating the growth of human prostate cancer cells.

Indexed as

AndrogensCell CommunicationCell DivisionCoculture TechniquesCulture Media, ConditionedEpithelial CellsExtracellular Signal-Regulated MAP KinasesFibroblastsHumansLuciferasesMaleMAP Kinase Signaling SystemPhosphorylationProstate-Specific AntigenProstatic NeoplasmsReceptors, AndrogenAndrogensAR protein, humanCulture Media, ConditionedExtracellular Signal-Regulated MAP KinasesLuciferasesProstate-Specific AntigenReceptors, AndrogenSerine

Identifiers

PMID19274665
PMCPMC2753603
OpenAlexW1981457098

What OpenQuestion holds

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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.