Evidence map›Paper›PMID 19502590›Full record

ArticleJournal of lipid research2009

Signaling through cholesterol esterification: a new pathway for the cholecystokinin 2 receptor involved in cell growth and invasion.

Michael R Paillasse, Philippe de Medina, Guillaume Amouroux, Loubna Mhamdi, Marc Poirot, Sandrine Silvente-Poirot

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.3field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Role ofJournal of Cancer · 2020
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Synergy of Dendritic Cell Vaccines and Avasimibe in Treatment of Head and Neck Cancer in Mice.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  20. Inhibition of SOAT1 Suppresses Glioblastoma Growth via Blocking SREBP-1-Mediated Lipogenesis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    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 3 institutions in 2 countries.

Michael R PaillasseINSERM 563, Equipe Métabolisme, Oncogenèse et Différenciation cellulaire, Centre de Physiopathologie de Toulouse Purpan, Institut Claudius Regaud, Toulouse France.
Philippe de Medina
Guillaume Amouroux
Loubna Mhamdi
Marc Poirot
Sandrine Silvente-Poirot
Centre de Physiopathologie de Toulouse-Purpan · FRUniversité Toulouse III - Paul Sabatier · FRInstitut Claudius Regaud · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several studies indicate that cholesterol esterification is deregulated in cancers. The present study aimed to characterize the role of cholesterol esterification in proliferation and invasion of two tumor cells expressing an activated cholecystokinin 2 receptor (CCK2R). A significant increase in cholesterol esterification and activity of Acyl-CoA:cholesterol acyltransferase (ACAT) was measured in tumor cells expressing a constitutively activated oncogenic mutant of the CCK2R (CCK2R-E151A cells) compared with nontumor cells expressing the wild-type CCK2R (CCK2R-WT cells). Inhibition of cholesteryl ester formation and ACAT activity by Sah58-035, an inhibitor of ACAT, decreased by 34% and 73% CCK2R-E151A cell growth and invasion. Sustained activation of CCK2R-WT cells by gastrin increased cholesteryl ester production while addition of cholesteryl oleate to the culture medium of CCK2R-WT cells increased cell proliferation and invasion to a level close to that of CCK2R-E151A cells. In U87 glioma cells, a model of autocrine growth stimulation of the CCK2R, inhibition of cholesterol esterification and ACAT activity by Sah58-035 and two selective antagonists of the CCK2R significantly reduced cell proliferation and invasion. In both models, cholesteryl ester formation was found dependent on protein kinase zeta/ extracellular signal-related kinase 1/2 (PKCzeta/ERK1/2) activation. These results show that signaling through ACAT/cholesterol esterification is a novel pathway for the CCK2R that contributes to tumor cell proliferation and invasion.

Indexed as

Cell ProliferationSignal TransductionAnimalsBenzodiazepinesBlotting, WesternCell Line, TumorCell MovementCholesterolCholesterol EstersEsterificationHormone AntagonistsHumansMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MutationBenzodiazepinesCholesterolCholesterol Esterscholesteryl oleateHormone AntagonistsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Protein Kinase CProtein Kinase C zetaReceptor, Cholecystokinin BSterol O-AcyltransferaseYM 022

Identifiers

PMID19502590
PMCPMC2759826
OpenAlexW1990913218

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.