Evidence map›Paper›PMID 24264576›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2014

GnRH-(1-5) transactivates EGFR in Ishikawa human endometrial cells via an orphan G protein-coupled receptor.

Madelaine Cho-Clark, Darwin O Larco, Nina N Semsarzadeh, Florencia Vasta, Shaila K Mani, T John Wu

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. GPR101 Mutations are not a Frequent Cause of Congenital Isolated Growth Hormone Deficiency.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2016
    Article
  19. Article
  20. GHRH excess and blockade in X-LAG syndrome.Endocrine-related cancer · 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 2 institutions in 1 country.

Madelaine Cho-ClarkDepartment of Obstetrics and Gynecology (T.J.W., M.C., F.V.) and the Program in Molecular and Cellular Biology (D.O.L., T.J.W.), Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814; and Departments of Molecular and Cellular Biology and Neuroscience (S.K.M.), Baylor College of Medicine, Houston, Texas 77030.
Darwin O Larco
Nina N Semsarzadeh
Florencia Vasta
Shaila K Mani
T John Wu
Uniformed Services University of the Health Sciences · USBaylor College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The decapeptide GnRH is known for its central role in the regulation of the hypothalamo-pituitary-gonadal axis. In addition, it is also known to have local effects within peripheral tissues. The zinc metalloendopeptidase, EC 3.4.24.15 (EP24.15), can cleave GnRH at the Tyr(5)-Gly(6) bond to form the pentapeptide, GnRH-(1-5). The central and peripheral effect of GnRH-(1-5) is different from its parent peptide, GnRH. In the current study, we examined the effect of GnRH-(1-5) on epidermal growth factor receptor (EGFR) phosphorylation and cellular migration. Using the Ishikawa cell line as a model of endometrial cancer, we demonstrate that GnRH-(1-5) stimulates epidermal growth factor release, increases the phosphorylation of EGFR (P < .05) at three tyrosine sites (992, 1045, 1068), and promotes cellular migration. In addition, we also demonstrate that these actions of GnRH-(1-5) are mediated by the orphan G protein-coupled receptor 101 (GPR101). Down-regulation of GPR101 expression blocked the GnRH-(1-5)-mediated release of epidermal growth factor and the subsequent phosphorylation of EGFR and cellular migration. These results suggest that GPR101 is a critical requirement for GnRH-(1-5) transactivation of EGFR in Ishikawa cells.

Indexed as

Transcriptional ActivationCalcium SignalingCell Line, TumorCell MovementEndometrial NeoplasmsEpidermal Growth FactorErbB ReceptorsFemaleGene ExpressionGonadotropin-Releasing HormoneHumansMatrix Metalloproteinase InhibitorsOligopeptidesOncogene ProteinsPeptide FragmentsPhenylalanineADGRF1 protein, humanbatimastatEGFR protein, humanEpidermal Growth FactorErbB ReceptorsGonadotropin-Releasing HormoneGPAnt-2GPR101 protein, humanLHRH (1-5)Matrix Metalloproteinase InhibitorsOligopeptidesOncogene ProteinsPeptide FragmentsPhenylalaninePyrrolidonecarboxylic AcidQuinazolinesReceptors, Cell SurfaceReceptors, G-Protein-CoupledReceptors, LHRHRTKI cpdThiophenesTyrphostins

Identifiers

PMID24264576
PMCPMC5426651
OpenAlexW2042435176

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.