Evidence map›Paper›PMID 21667400›Full record

ArticleNutrition and cancer2011

Omega-3 fatty acid inhibition of prostate cancer progression to hormone independence is associated with suppression of mTOR signaling and androgen receptor expression.

William Friedrichs, Shivani B Ruparel, Robert A Marciniak, Linda deGraffenried

Open access · greenAbstract readComparative Study
In one paragraph

Article in Nutrition and cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.0field-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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Cholesterol as a metabolic integrator of oncogenic signaling, immune evasion, and therapy resistance.Apoptosis : an international journal on programmed cell death · 2026
    Review
  3. Review
  4. Anticancer Effect ofMolecules (Basel, Switzerland) · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Dietary Carcinogens and DNA Adducts in Prostate Cancer.Advances in experimental medicine and biology · 2019
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  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

4 authors at 2 institutions in 1 country.

William FriedrichsDepartment of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Shivani B Ruparel
Robert A Marciniak
Linda deGraffenried
The University of Texas Health Science Center at San Antonio · USThe University of Texas at Austin · US

Funding

Dietary Prevention of Hormone Refractory Prostate CancerR03CA099115 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI DE GRAFFENRIED, LINDA A · 2003 to 2004
$146k
NCI NIH HHS CA099115NCI NIH HHS R03 CA099115
6 · The paper itself

Abstract

Currently, progression of prostate cancer to androgen independence remains the primary obstacle to improved survival. In order to improve overall survival, novel treatment strategies that are based upon specific molecular mechanisms that prolong the androgen-dependent state and that are useful for androgen-independent disease need to be identified. Both epidemiological as well as preclinical data suggest that omega-3 fatty acids are effective primary tumor prevention agents; however, their efficacy at preventing and treating refractory prostate cancer has not been as thoroughly investigated. We used an in vitro model of androgen ablation to determine the effect of treatment with omega-3 fatty acids on the progression to an androgen-independent state. The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) were able to prevent progression of LNCaP cells while the omega-6 fatty acid arachidonic acid (AA) actually promoted cell growth under conditions of hormone depletion. These results correlated with a decrease in the expression of the androgen receptor as well as suppression of the Akt/mTOR signaling pathway. Connecting the mechanisms by which omega-3 fatty acids affect phenotypic outcome is important for effective exploitation of these nutrient agents as a therapeutic approach. Understanding these processes is critical for the development of effective dietary intervention strategies that improve overall survival.

Indexed as

Signal TransductionAndrogensCell Line, TumorCell ProliferationClone CellsDocosahexaenoic AcidsEicosapentaenoic AcidFatty Acids, Omega-3HumansMaleNeoplasm ProteinsPhosphorylationProstatic NeoplasmsProtein Processing, Post-TranslationalProto-Oncogene Proteins c-aktReceptors, AndrogenAndrogensAR protein, humanDocosahexaenoic AcidsEicosapentaenoic AcidFatty Acids, Omega-3MTOR protein, humanNeoplasm ProteinsProto-Oncogene Proteins c-aktReceptors, AndrogenTOR Serine-Threonine Kinases

Identifiers

PMID21667400
PMCPMC12155126
OpenAlexW1967697680

What OpenQuestion holds

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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.