Evidence map›Paper›PMID 11577170›Full record

ArticleMolecular pathology : MP2001

Inhibition of glioma cell growth and tumorigenic potential by CCN3 (NOV).

N Gupta, H Wang, T L McLeod, C C Naus, S Kyurkchiev, S Advani, J Yu, B Perbal, R R Weichselbaum

Open access · bronzeAbstract read
In one paragraph

Article in Molecular pathology : MP, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

43 citing papers in PubMed, 105 citations in OpenAlex.

  1. Article
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Human pancreatic cancer progression: an anarchy among CCN-siblings.Journal of cell communication and signaling · 2016
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. CCN proteins: A centralized communication network.Journal of cell communication and signaling · 2013
    Article
  19. Article
  20. Gap junctions.Comprehensive Physiology · 2012
    Review
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

9 authors at 5 institutions in 3 countries.

N GuptaDepartment of Surgery, University of Chicago, Chicago IL 60637, USA.
H Wang
T L McLeod
C C Naus
S Kyurkchiev
S Advani
J Yu
B Perbal
R R Weichselbaum
Délégation Paris 7 · FRUniversité Paris Cité · FRUniversity of Chicago · USWestern University · CALaboratoire d'Electrochimie Moléculaire · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsTo establish whether the ectopic expression of CCN3 (NOV) in glioma cells can interfere with their tumorigenic potential and assess its potential value in molecular medicine.

methodsGlioma cell lines were used to assess whether differences in the degree of intracellular communication induced by the expression of the gap junction protein connexin 43 (Cx43) is related to the differential expression of CCN3 (NOV). The antiproliferative activity of rat CCN3 (rCCN3; NOV) in glioma cells, has been assessed both in vitro and in vivo with glioma cell lines expressing different amounts of CCN3 (NOV).

resultsUpon ectopic expression of Cx43, the growth of C6 glioma cells is decreased. An increase of CCN3 (NOV) expression matches the reduced tumorigenic potential of these transfected cells. The localisation of CCN3 (NOV) is affected by the increased expression of Cx43 in the Cx-13 transfected cells, in which it is detected at areas of cell-cell contact. In a xenograft model, CCN3 (NOV) transfected glioma cells were found to induce tumours to a lesser degree than their parental counterparts, which do not express detectable amounts of CCN3 (NOV).

conclusionsPrevious observations had suggested an inverse relation between CCN3 (NOV) expression in glioma cells and their tumorigenicity. These results establish a direct association between the establishment of functional gap junctional intercellular communication and the expression of rCCN3 (NOV). In addition to a negative effect on murine and human cell growth, CCN3 (NOV) has antiproliferative activity on tumour cells in vivo. Thus, the antiproliferative activity of the CCN3 (NOV) protein might involve reorganisation of cellular contacts that play a crucial role in tumorigenesis. The antiproliferative activity of CCN3 (NOV) established in this work sets the stage for the potential use of CCN proteins in molecular oncology.

Indexed as

AnimalsCell CommunicationCell DivisionConnexin 43FemaleGene ExpressionGliomaHumansMiceMice, NudeModels, AnimalRatsRepressor ProteinsReverse Transcriptase Polymerase Chain ReactionTransfectionTumor Cells, CulturedConnexin 43Repressor Proteins

Identifiers

PMID11577170
PMCPMC1187085
OpenAlexW2126111920

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Registered trials

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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.