Evidence map›Paper›PMID 20660502›Full record

ArticleCarcinogenesis2010

Cannabinoid receptor-dependent and -independent anti-proliferative effects of omega-3 ethanolamides in androgen receptor-positive and -negative prostate cancer cell lines.

Iain Brown, Maria G Cascio, Klaus W J Wahle, Reem Smoum, Raphael Mechoulam, Ruth A Ross, Roger G Pertwee, Steven D Heys

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
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  9. Need for Methods to Investigate Endocannabinoid Signaling.Methods in molecular biology (Clifton, N.J.) · 2023
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  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Peroxisomal ABC Transporters: An Update.International journal of molecular sciences · 2021
    Review
  16. Two NewBiomedicines · 2021
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  17. Article
  18. Bioactive Lipids in MSCs Biology: State of the Art and Role in Inflammation.International journal of molecular sciences · 2021
    Review
  19. GPR55 Receptor Activation by theInternational journal of molecular sciences · 2021
    Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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 3 countries.

Iain BrownCancer Medicine Research Programme, Translational Medical Sciences, Division of Applied Medicine, School of Medicine and Dentistry, University of Aberdeen, Polwarth Building, Aberdeen, AB25 2ZD, UK. i.brown@abdn.ac.uk
Maria G Cascio
Klaus W J Wahle
Reem Smoum
Raphael Mechoulam
Ruth A Ross
Roger G Pertwee
Steven D Heys
University of Aberdeen · GBHebrew University of Jerusalem · ILNutrition Sciences (Belgium) · BE

Funding

SYNTHESIS OF SR141716A AND ANANDAMIDE ANALOGSP01DA009789 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI CRAVATT, BENJAMIN F · 1995 to 2013
$11.6M
NIDA NIH HHS DA-009789
6 · The paper itself

Abstract

The omega-3 fatty acid ethanolamides, docosahexaenoyl ethanolamide (DHEA) and eicosapentaenoyl ethanolamide (EPEA), displayed greater anti-proliferative potency than their parent omega-3 fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), in LNCaP and PC3 prostate cancer cells. DHEA and EPEA activated cannabinoid CB(1) and CB(2) receptors in vitro with significant potency, suggesting that they are endocannabinoids. Both LNCaP and PC3 cells expressed CB(1) and CB(2) receptors, and the CB(1)- and CB(2)-selective antagonists, AM281 and AM630, administered separately or together, reduced the anti-proliferative potencies of EPEA and EPA but not of DHEA or DHA in PC3 cells and of EPA but not of EPEA, DHEA or DHA in LNCaP cells. Even so, EPEA and EPA may not have inhibited PC3 or LNCaP cell proliferation via cannabinoid receptors since the anti-proliferative potency of EPEA was well below the potency it displayed as a CB(1) or CB(2) receptor agonist. Indeed, these receptors may mediate a protective effect because the anti-proliferative potency of DHEA in LNCaP and PC3 cells was increased by separate or combined administration of AM281 and AM630. The anandamide-metabolizing enzyme, fatty acid amide hydrolase (FAAH), was highly expressed in LNCaP but not PC3 cells. Evidence was obtained that FAAH metabolizes EPEA and DHEA and that the anti-proliferative potencies of these ethanolamides in LNCaP cells can be enhanced by inhibiting this enzyme. Our findings suggest that the expression of cannabinoid receptors and of FAAH in some tumour cells could well influence the effectiveness of DHA and EPA or their ethanolamide derivatives as anticancer agents.

Indexed as

Adjuvants, ImmunologicAmidohydrolasesAnimalsApoptosisBlotting, WesternCell CycleCell MembraneCell ProliferationCHO CellsCricetinaeCricetulusDehydroepiandrosteroneFatty Acid Amide HydrolasesFatty Acids, Omega-3Flow CytometryHumansAdjuvants, ImmunologicAmidohydrolasesDehydroepiandrosteroneFatty Acid Amide HydrolasesFatty Acids, Omega-3Receptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2Receptors, AndrogenRNA, Messenger

Identifiers

PMID20660502
PMCPMC2930808
OpenAlexW2111775116

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.