Evidence map›Paper›PMID 19154441›Full record

ArticleBritish journal of pharmacology2009

Eicosapentaenoic acid inhibits voltage-gated sodium channels and invasiveness in prostate cancer cells.

T Nakajima, N Kubota, T Tsutsumi, A Oguri, H Imuta, T Jo, H Oonuma, M Soma, K Meguro, H Takano and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  12. KPflugers Archiv : European journal of physiology · 2016
    Article
  13. Sigma-1 receptors modulate neonatal NaEuropean biophysics journal : EBJ · 2016
    Article
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  15. Article
  16. Review
  17. Dual roles of voltage-gated sodium channels in development and cancer.The International journal of developmental biology · 2015
    Review
  18. Regulation of voltage-gated sodium channel expression in cancer: hormones, growth factors and auto-regulation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Review
  19. Article
  20. 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

12 authors at 5 institutions in 1 country.

T NakajimaDepartment of Ischemic Circulatory Physiology, The University of Tokyo, Japan. masamasa@pb4.so-net.ne.jp
N Kubota
T Tsutsumi
A Oguri
H Imuta
T Jo
H Oonuma
M Soma
K Meguro
H Takano
T Nagase
T Nagata
The University of Tokyo · JPUniversity of Tokyo Hospital · JPHamamatsu University School of Medicine · JPMochida Pharmaceutical (Japan) · JPShowa University Fujigaoka Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeThe voltage-gated Na(+) channels (Na(v)) and their corresponding current (I(Na)) are involved in several cellular processes, crucial to metastasis of cancer cells. We investigated the effects of eicosapentaenoic (EPA), an omega-3 polyunsaturated fatty acid, on I(Na) and metastatic functions (cell proliferation, endocytosis and invasion) in human and rat prostate cancer cell lines (PC-3 and Mat-LyLu cells). EXPERIMENTAL APPROACH: The whole-cell voltage clamp technique and conventional/quantitative real-time reverse transcriptase polymerase chain reaction analysis were used. The presence of Na(v) proteins was shown by immunohistochemical methods. Alterations in the fatty acid composition of phospholipids after treatment with EPA and metastatic functions were also examined. KEY

resultsA transient inward Na(+) current (I(Na)), highly sensitive to tetrodotoxin, and Na(V) proteins were found in these cells. Expression of Na(V)1.6 and Na(V)1.7 transcripts (SCN8A and SCN9A) was predominant in PC-3 cells, while Na(V)1.7 transcript (SCN9A) was the major component in Mat-LyLu cells. Tetrodotoxin or synthetic small interfering RNA targeted for SCN8A and SCN9A inhibited metastatic functions (endocytosis and invasion), but failed to inhibit proliferation in PC-3 cells. Exposure to EPA produced a rapid and concentration-dependent suppression of I(Na). In cells chronically treated (up to 72h) with EPA, the EPA content of cell lipids increased time-dependently, while arachidonic acid content decreased. Treatment of PC-3 cells with EPA decreased levels of mRNA for SCN9A and SCN8A, cell proliferation, invasion and endocytosis. CONCLUSION AND IMPLICATIONS: Treatment with EPA inhibited I(Na) directly and also indirectly, by down-regulation of Na(v) mRNA expression in prostate cancer cells, thus inhibiting their metastatic potential.

Indexed as

AnimalsCell Line, TumorCell MovementCell ProliferationEicosapentaenoic AcidEndocytosisGene ExpressionHumansImmunoblottingIon Channel GatingMaleNeoplasm InvasivenessPatch-Clamp TechniquesProstatic NeoplasmsRatsReverse Transcriptase Polymerase Chain ReactionEicosapentaenoic AcidRNA, Small InterferingSodium Channels

Identifiers

PMID19154441
PMCPMC2697676
OpenAlexW2072291790

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.