Evidence map›Paper›PMID 19920825›Full record

ArticleBritish journal of cancer2009

Epac inhibits migration and proliferation of human prostate carcinoma cells.

M Grandoch, A Rose, M ter Braak, V Jendrossek, H Rübben, J W Fischer, M Schmidt, A A Weber

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

37 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. High PGEScientifica · 2026
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  7. The Role of Epac in Cancer Progression.International journal of molecular sciences · 2020
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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 3 institutions in 2 countries.

M GrandochDepartment of Pharmacology, University of Essen Medical School, Essen, Germany. maria.grandoch@uk-essen.de
A Rose
M ter Braak
V Jendrossek
H Rübben
J W Fischer
M Schmidt
A A Weber
Essen University Hospital · DEUniversity of Duisburg-Essen · DEUniversity of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt was recently found that cAMP mediates protein kinase A-independent effects through Epac proteins. The aim of this study was to investigate the role of Epac in migration and proliferation of prostate carcinoma cells.

methodsThe effect of Epac activation was determined by [(3)H]thymidine incorporation and scratch assays in PC-3 and DU 145 cells. Furthermore, cytoskeletal integrity was analysed by phalloidin staining. The participation of intracellular Epac effectors such as mitogen-activated protein (MAP) kinases, Rap1- and Rho-GTPases was determined by immunoblotting and pull-down assay.

resultsThe specific Epac activator 8-pCPT-2'-O-Me-cAMP (8-pCPT) interfered with cytoskeletal integrity, reduced DNA synthesis, and migration. Although 8-pCPT activated Rap1, it inhibited MAP kinase signalling and RhoA activation. These findings were translated into functional effects such as inhibition of mitogenesis, cytoskeletal integrity, and migration.

conclusionIn human prostate carcinoma cells, Epac inhibits proliferative and migratory responses likely because of inhibition of MAP kinase and RhoA signalling pathways. Therefore, Epac might represent an attractive therapeutic target in the treatment of prostate cancer.

Indexed as

ActinsCadherinsCell Line, TumorCell MovementCell ProliferationCyclic AMPGuanine Nucleotide Exchange FactorsHumansMaleProstatic NeoplasmsrhoA GTP-Binding Protein8-(4-chloro-phenylthio)-2'-O-methyladenosine-3'-5'-cyclic monophosphateActinsCadherinsCyclic AMPGuanine Nucleotide Exchange FactorsRAPGEF3 protein, humanrhoA GTP-Binding Protein

Identifiers

PMID19920825
PMCPMC2795436
OpenAlexW1975834956

What OpenQuestion holds

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LicenceCC BY
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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.