Evidence map›Paper›PMID 18205914›Full record

ArticleBMC cancer2008

Loss of Endocan tumorigenic properties after alternative splicing of exon 2.

Florence Depontieu, Bogdan-Dragos Grigoriu, Arnaud Scherpereel, Estelle Adam, Maryse Delehedde, Philippe Gosset, Philippe Lassalle

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

10 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Endocan and the respiratory system: a review.International journal of chronic obstructive pulmonary disease · 2016
    Review
  7. Article
  8. Article
  9. Article
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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

7 authors at 2 institutions in 2 countries.

Florence DepontieuINSERM U774, Lille 59019, France. fdepont2@jhmi.edu
Bogdan-Dragos Grigoriu
Arnaud Scherpereel
Estelle Adam
Maryse Delehedde
Philippe Gosset
Philippe Lassalle
Inserm · FRInstitut Pasteur de Lille · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndocan was originally described as a dermatan sulfate proteoglycan found freely circulating in the blood. Endocan expression confers tumorigenic properties to epithelial cell lines or accelerate the growth of already tumorigenic cells. This molecule is the product of a single gene composed of 3 exons. Previous data showed that endocan mRNA is subject to alternative splicing with possible generation of two protein products. In the present study we identified, and functionally characterized, the alternative spliced product of the endocan gene: the exon 2-deleted endocan, called endocanDelta2.

methodsStable, endocanDelta2-overexpressing cell lines were generated to investigate the biological activities of this new alternatively spliced product of endocan gene. Tumorigenesis was studied by inoculating endocan and endocanDelta2 expressing cell lines subcutaneously in SCID mice. Biochemical properties of endocan and endocanDelta2 were studied after production of recombinant proteins in various cell lines of human and murine origin.

resultsOur results showed that the exon 2 deletion impairs synthesis of the glycan chain, known to be involved in the pro-tumoral effect of endocan. EndocanDelta2 did not promote tumor formation by 293 cells implanted in the skin of severe combined immunodeficient (SCID) mice.

conclusionOur results emphasize the key role of the polypeptide sequence encoded by the exon 2 of endocan gene in tumorigenesis, and suggest that this sequence could be a target for future therapies against cancer.

Indexed as

Alternative SplicingAnimalsCell Transformation, NeoplasticCHO CellsCricetinaeCricetulusDNA, ComplementaryEndothelial CellsExonsGene DeletionHumansLung NeoplasmsMiceMice, SCIDNeoplasm ProteinsPolysaccharidesDNA, ComplementaryESM1 protein, humanNeoplasm ProteinsPolysaccharidesProtein IsoformsProteoglycansRNA, Messenger

Identifiers

PMID18205914
PMCPMC2254430
OpenAlexW1991044670

What OpenQuestion holds

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LicenceCC BY
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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.