Evidence map›Paper›PMID 22343623›Full record

ArticleBritish journal of cancer2012

Effect of κ-opioid receptor agonist on the growth of non-small cell lung cancer (NSCLC) cells.

N Kuzumaki, A Suzuki, M Narita, T Hosoya, A Nagasawa, S Imai, K Yamamizu, H Morita, H Nagase, Y Okada and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. NovelJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2018
    Article
  16. Article
  17. Article
  18. Chronic opioid therapy in long-term cancer survivors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017
    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

15 authors at 6 institutions in 1 country.

N KuzumakiDepartment of Physiology, Keio University, School of Medicine, 35 Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan.
A Suzuki
M Narita
T Hosoya
A Nagasawa
S Imai
K Yamamizu
H Morita
H Nagase
Y Okada
H J Okano
J K Yamashita
H Okano
T Suzuki
M Narita
Ebara (Japan) · JPKeio University Hospital · JPHoshi University · JPKyoto University · JPJapan Biological Informatics Consortium · JPKitasato University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt is becoming increasingly recognised that opioids are responsible for tumour growth. However, the effects of opioids on tumour growth have been controversial.

methodsThe effects of κ-opioid receptor (KOR) agonist on the growth of non-small cell lung cancer (NSCLC) cells were assessed by a cell proliferation assay. Western blotting was performed to ascertain the mechanism by which treatment with KOR agonist suppresses tumour growth.

resultsAddition of the selective KOR agonist U50,488H to gefitinib-sensitive (HCC827) and gefitinib-resistant (H1975) NSCLC cells produced a concentration-dependent decrease in their growth. These effects were abolished by co-treatment with the selective KOR antagonist nor-BNI. Furthermore, the growth-inhibitory effect of gefitinib in HCC827 cells was further enhanced by co-treatment with U50,488H. With regard to the inhibition of tumour growth, the addition of U50, 488H to H1975 cells produced a concentration-dependent decrease in phosphorylated-glycogen synthase kinase 3β (p-GSK3β).

conclusionThe present results showed that stimulation of KOR reduces the growth of gefitinib-resistant NSCLC cells through the activation of GSK3β.

Indexed as

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-IsomerAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCell SurvivalDrug Resistance, NeoplasmErbB ReceptorsGefitinibGene ExpressionGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansMutation, MissenseNaltrexonePhosphorylation3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-IsomerAntineoplastic AgentsErbB ReceptorsGefitinibGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanNaltrexonenorbinaltorphimineProto-Oncogene Proteins c-aktQuinazolinesReceptors, Opioid, kappaSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID22343623
PMCPMC3304401
OpenAlexW2050008870

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.