Evidence map›Paper›PMID 25575808›Full record

ArticleOncotarget2015

The non glycanated endocan polypeptide slows tumor growth by inducing stromal inflammatory reaction.

Hanane Yassine, Nathalie De Freitas Caires, Florence Depontieu, Arnaud Scherpereel, Ali Awad, Anne Tsicopoulos, Christophe Leboeuf, Anne Janin, Catherine Duez, Bogdan Grigoriu and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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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

11 authors at 6 institutions in 2 countries.

Hanane YassineInstitut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France.
Nathalie De Freitas CairesInstitut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France.
Florence DepontieuInstitut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France.
Arnaud ScherpereelInstitut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France.
Ali AwadInstitut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France.
Anne TsicopoulosInstitut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France.
Christophe LeboeufInstitut National de la Santé et de la Recherche Médicale, Paris, France.
Anne JaninInstitut National de la Santé et de la Recherche Médicale, Paris, France.
Catherine DuezInstitut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France.
Bogdan GrigoriuInstitut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France.
Philippe LassalleInstitut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France.
Institut Pasteur de Lille · FRCentre National de la Recherche Scientifique · FRInserm · FRUniversité Lille Nord de France · FRCenter for Infection and Immunity of Lille · FRUniversité de Lille · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endocan expression is increasingly studied in various human cancers. Experimental evidence showed that human endocan, through its glycan chain, is implicated in various processes of tumor growth. We functionally characterize mouse endocan which is also a chondroitin sulfate proteoglycan but much less glycanated than human endocan. Distant domains from the O-glycanation site, located within exons 1 and 2 determine the glycanation pattern of endocan. In opposite to the human homologue, overexpression of mouse endocan in HT-29 cells delayed the tumor appearance and reduced the tumor growth rate. This tumor growth inhibition is supported by non glycanated form of mouse endocan. Non glycanated human endocan overexpressed in HT-29, A549 or K1000 cells also exhibited an anti-tumor effect. Moreover, systemic delivery of non glycanated human endocan also results in HT-29 tumor growth delay. In vitro, endocan polypeptide did not affect HT-29 cell proliferation, nor cell viability. In tumor tissue sections, a stromal inflammatory reaction was observed only in tumors overexpressing endocan polypeptide, and depletion of CD122+ cells was able to delete partially the anti-tumor effect of endocan polypeptide. These results reveal a novel pathway for endocan in the control of tumor growth, which involves inflammatory cells of the innate immunity.

Indexed as

AnimalsCell ProliferationCHO CellsColonic NeoplasmsCricetulusGenetic TherapyGlycosylationHEK293 CellsHT29 CellsHumansImmunity, InnateInflammationInterleukin-2 Receptor beta SubunitMaleMiceMice, SCIDendothelial cell-specific molecule-1, mouseESM1 protein, humanInterleukin-2 Receptor beta SubunitNeoplasm ProteinsProteoglycans

Identifiers

PMID25575808
PMCPMC4413613
OpenAlexW1868383766

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.