Evidence map›Paper›PMID 28350804›Full record

ArticlePloS one2017

Syndecan-1 deficiency promotes tumor growth in a murine model of colitis-induced colon carcinoma.

Adi Binder Gallimidi, Gabriel Nussbaum, Esther Hermano, Barak Weizman, Amichay Meirovitz, Israel Vlodavsky, Martin Götte, Michael Elkin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  4. Matrix proteoglycans in tumor inflammation and immunity.American journal of physiology. Cell physiology · 2022
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  12. Heparanase-enhanced Shedding of Syndecan-1 and Its Role in Driving Disease Pathogenesis and Progression.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020
    Review
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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

8 authors at 2 institutions in 1 country.

Adi Binder GallimidiSharett Oncology Institute, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Gabriel NussbaumInstitute of Dental Sciences, Hebrew University-Hadassah Faculty of Dental Medicine, Jerusalem, Israel.
Esther HermanoSharett Oncology Institute, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Barak WeizmanSharett Oncology Institute, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Amichay MeirovitzSharett Oncology Institute, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Israel VlodavskyCancer and Vascular Biology Research Center, The Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Martin GötteDepartment of Gynecology and Obstetrics, Muenster University, Medical Center, Muenster Germany.
Michael ElkinSharett Oncology Institute, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Hadassah Medical Center · ILHebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Syndecan-1 (Sdc1) is an important member of the cell surface heparan sulfate proteoglycan family, highly expressed by epithelial cells in adult organisms. Sdc1 is involved in the regulation of cell migration, cell-cell and cell-matrix interactions, growth-factor, chemokine and integrin activity, and implicated in inflammatory responses and tumorigenesis. Gastrointestinal tract represents an important anatomic site where loss of Sdc1 expression was reported both in inflammation and malignancy. However, the biological significance of Sdc1 in chronic colitis-associated tumorigenesis has not been elucidated. To the best of our knowledge, this study is the first to test the effects of Sdc1 loss on colorectal tumor development in inflammation-driven colon tumorigenesis. Utilizing a mouse model of colitis-related colon carcinoma induced by the carcinogen azoxymethane (AOM), followed by the inflammatory agent dextran sodium sulfate (DSS), we found that Sdc1 deficiency results in increased susceptibility to colitis-associated tumorigenesis. Importantly, colitis-associated tumors developed in Sdc1-defficient mice were characterized by increased local production of IL-6, activation of STAT3, as well as induction of several STAT3 target genes that act as important effectors of colonic tumorigenesis. Altogether, our results highlight a previously unknown effect of Sdc1 loss in progression of inflammation-associated cancer and suggest that decreased levels of Sdc1 may serve as an indicator of colon carcinoma progression in the setting of chronic inflammation.

Indexed as

Gene DeletionAnimalsCarcinogenesisColitisColonColonic NeoplasmsDisease Models, AnimalGene Expression Regulation, NeoplasticMaleMice, Inbred C57BLMice, KnockoutSyndecan-1Syndecan-1

Identifiers

PMID28350804
PMCPMC5369774
OpenAlexW2598583594

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.