Evidence map›Paper›PMID 20663860›Full record

ArticleMolecular cancer research : MCR2010

Oxytocin induces the migration of prostate cancer cells: involvement of the Gi-coupled signaling pathway.

Miao Zhong, Maryam L Boseman, Ana C Millena, Shafiq A Khan

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
6.4field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Suppression of GNAI2 message in ovarian cancer.Journal of ovarian research · 2014
    Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. OXTRNature communications · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Oxytocin and cancer: An emerging link.World journal of clinical oncology · 2018
    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

4 authors at 2 institutions in 1 country.

Miao ZhongCenter for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, GA 30314, USA.
Maryam L Boseman
Ana C Millena
Shafiq A Khan
Center for Cancer Research · USClark Atlanta University · US

Funding

THEORY OF PLANNED BEHAVIOR VS ETHNICITY /PHYSICAL ACTIVIG12RR003062 · NCRR · CLARK ATLANTA UNIVERSITY · PI BROWN, CARLTON B · 1985 to 2011
$15.5M
TRAINNING COREP20MD002285 · NIMHD · CLARK ATLANTA UNIVERSITY · PI CHAUDHARY, JAIDEEP · 2007 to 2016
$10.9M
NCRR NIH HHS 5G12RR003062NCRR NIH HHS G12 RR003062NIMHD NIH HHS 1P20MD002285-01NIMHD NIH HHS P20 MD002285
6 · The paper itself

Abstract

Expression of genes that encode oxytocin (OXT) and vasopressin (AVP) and their cognate receptors in normal and diseased prostates are only partially characterized. Reverse transcription and PCR were used to examine the expression of these genes in normal prostate epithelial and stromal cell lines, k-ras-transformed prostate epithelial cell lines, and in four prostate cancer cell lines. Secreted and cell-associated OXT peptide was measured by an enzyme immunoassay. OXT and its receptor (OXTR) were expressed in all eight prostate cell lines. Cell-associated OXT peptide was also found in all prostate epithelial cell lines except in DU145 cells. Neither AVP nor its cognate receptors (V1a receptor and V2 receptor) were expressed in any prostate cell line examined. These data point to the OXTR as the primary target of OXT and AVP, and suggest that OXT might be an autocrine/paracrine regulator in human prostate. We found that OXT induces the migration of PC3 and PC3M, but not DU145 prostate cancer cells. The effect of OXT is distinct from the epidermal growth factor (EGF)-induced migration of prostate cancer cells, in which ERK1/2 and EGF receptor kinase activities were required. When cells were pretreated with pertussis toxin, the effect of OXT, but not EGF, on cell migration was abolished. Pretreatment with the cyclic AMP analogue, 8-Br-cAMP, did not affect OXT-induced cell migration, which eliminated the nonspecific effect of pertussis toxin. We conclude that a Gi-dependent mechanism is involved in OXTR-mediated migration of prostate cancer cells, and indicates a role for OXTR in prostate cancer metastasis.

Indexed as

Blotting, WesternCell AdhesionCell MovementCell ProliferationCells, CulturedErbB ReceptorsGTP-Binding Protein alpha Subunits, Gi-GoHumansMaleOxytocicsOxytocinPeptide FragmentsPertussis ToxinProstatic NeoplasmsReceptors, OxytocinReverse Transcriptase Polymerase Chain ReactionEGFR protein, humanErbB ReceptorsGTP-Binding Protein alpha Subunits, Gi-GoOxytocicsOxytocinPeptide FragmentsPertussis ToxinReceptors, OxytocinRNA, MessengerVasoconstrictor AgentsVasopressins

Identifiers

PMID20663860
PMCPMC2923666
OpenAlexW2136165616

What OpenQuestion holds

Textmetadata
LicenceTDM
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.