Evidence map›Paper›PMID 18320072›Full record

ArticleNeoplasia (New York, N.Y.)2008

Differential expression of secretory phospholipases A2 in normal and malignant prostate cell lines: regulation by cytokines, cell signaling pathways, and epigenetic mechanisms.

Mario Menschikowski, Albert Hagelgans, Eugene Gussakovsky, Heike Kostka, Elena L Paley, Gabriele Siegert

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Epigenetic control of group V phospholipase A2 expression in human malignant cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  6. Review
  7. Serum amyloid A, phospholipase A₂-IIA and C-reactive protein as inflammatory biomarkers for prostate diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. The War on Cancer rages on.Neoplasia (New York, N.Y.) · 2009
    Article
  16. Article
  17. Article
  18. Neoplasia: the second decade.Neoplasia (New York, N.Y.) · 2008
    Article
  19. 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 4 institutions in 3 countries.

Mario MenschikowskiTechnische Universität Dresden, Medizinische Fakultät Carl Gustav Carus, Institut für Klinische Chemie und Laboratoriumsmedizin, Dresden, Germany. menschik@rcs.urz.tu-dresden.de
Albert Hagelgans
Eugene Gussakovsky
Heike Kostka
Elena L Paley
Gabriele Siegert
TU Dresden · DEBiomed Research Institute · USNational Research Council Canada · CAUniversity Hospital Carl Gustav Carus · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upregulation of group IIA phospholipase A(2) (sPLA(2)-IIA) correlates with prostate tumor progression suggesting prooncogenic properties of this protein. Here, we report data on expression of three different sPLA(2) isozymes (groups IIA, V, and X) in normal (PrEC) and malignant (DU-145, PC-3, and LNCaP) human prostate cell lines. All studied cell lines constitutively expressed sPLA(2)-X, whereas sPLA(2)-V transcripts were identified only in malignant cells. In contrast, no expression of sPLA(2)-IIA was found in PrEC and DU-145 cells, but it was constitutively expressed by IFN-gamma in LNCaP and PC-3 cells. Expression of sPLA(2)-IIA is upregulated in PC-3 and in PrEC cell in a signal transducer and activator of transcription-1-dependent manner, but not in LNCaP cell. Additional signaling pathways regulating sPLA(2)-IIA expression include cAMP/protein kinase A, p38 mitogen-activated protein kinase, protein kinase C, Rho-kinase, and mitogen-activated/extracellular response protein kinase / extracellular signal-regulated kinase. No deletions were revealed in the sPLA(2)-IIA gene from DU-145 cells lacking the expression of sPLA(2)-IIA. Reexpression of sPLA(2)-IIA was induced by 5-aza-2'-deoxycytidine demonstrating that DNA methylation is implicated in the regulation of sPLA(2)-II. Together, these data suggest that sPLA(2)-IIA and sPLA(2)-V, but not sPLA(2)-X, are differentially expressed in normal and malignant prostate cells under the control of proinflammatory cytokines; epigenetic mechanisms appear involved in the regulation of sPLA(2)-IIA expression, at least in DU-145 cells.

Indexed as

Epigenesis, GeneticGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticCell Line, TumorCytokinesDNA Modification MethylasesGroup II Phospholipases A2Group V Phospholipases A2Group X Phospholipases A2HumansInterferon-gammaIsoenzymesMaleProstateProstatic NeoplasmsSignal TransductionCytokinesDNA Modification MethylasesGroup II Phospholipases A2Group V Phospholipases A2Group X Phospholipases A2Interferon-gammaIsoenzymesTranscription Factors

Identifiers

PMID18320072
PMCPMC2259456
OpenAlexW1524698046

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.