Evidence map›Paper›PMID 22815940›Full record

ArticlePloS one2012

Reduced susceptibility to colitis-associated colon carcinogenesis in mice lacking plasma membrane-associated sialidase.

Kazunori Yamaguchi, Kazuhiro Shiozaki, Setsuko Moriya, Koichi Koseki, Tadashi Wada, Hiroo Tateno, Ikuro Sato, Masahide Asano, Yoichiro Iwakura, Taeko Miyagi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 61 citations in OpenAlex.

  1. iScience · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. Inhibitors of the Sialidase NEU3 as Potential Therapeutics for Fibrosis.International journal of molecular sciences · 2022
    Review
  6. Review
  7. Neu3 neuraminidase induction triggers intestinal inflammation and colitis in a model of recurrent human food-poisoning.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  8. The Role of Glycosyltransferases in Colorectal Cancer.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Inhibiting Sialidase-Induced TGF-The Journal of pharmacology and experimental therapeutics · 2021
    Article
  11. Article
  12. Article
  13. Attenuated pulmonary fibrosis in sialidase-3 knockout (American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. 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

10 authors at 6 institutions in 1 country.

Kazunori YamaguchiDivision of Molecular and Cellular Oncology, Miyagi Cancer Center Research Institute, Natori, Japan. kyamaguchi@med.tohoku.ac.jp
Kazuhiro Shiozaki
Setsuko Moriya
Koichi Koseki
Tadashi Wada
Hiroo Tateno
Ikuro Sato
Masahide Asano
Yoichiro Iwakura
Taeko Miyagi
Miyagi Prefectural Hospital Organization · JPTohoku Medical and Pharmaceutical University · JPKagoshima University · JPKanazawa University · JPSystems Biology Institute · JPTochigi Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sialic acids are acidic monosaccharides that bind to the sugar chains of glycoconjugates and change their conformation, intermolecular interactions, and/or half-life. Thus, sialidases are believed to modulate the function of sialoglycoconjugates by desialylation. We previously reported that the membrane-associated mammalian sialidase NEU3, which preferentially acts on gangliosides, is involved in cell differentiation, motility, and tumorigenesis. The NEU3 gene expression is aberrantly elevated in several human cancers, including colon, renal, prostate, and ovarian cancers. The small interfering RNA-mediated knock-down of NEU3 in cancer cell lines, but not in normal cell-derived primary cultures, downregulates EGFR signaling and induces apoptosis. Here, to investigate the physiological role of NEU3 in tumorigenesis, we established Neu3-deficient mice and then subjected them to carcinogen-induced tumorigenesis, using a sporadic and a colitis-associated colon cancer models. The Neu3-deficient mice showed no conspicuous accumulation of gangliosides in the brain or colon mucosa, or overt abnormalities in their growth, development, behavior, or fertility. In dimethylhydrazine-induced colon carcinogenesis, there were no differences in the incidence or growth of tumors between the Neu3-deficient and wild-type mice. On the other hand, the Neu3-deficient mice were less susceptible than wild-type mice to the colitis-associated colon carcinogenesis induced by azoxymethane and dextran sodium sulfate. These results suggest that NEU3 plays an important role in inflammation-dependent tumor development.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAzoxymethaneCell MembraneColitisColonic NeoplasmsDextransGangliosidesGene Expression ProfilingGenetic Predisposition to DiseaseGenetic VectorsGenotypeGlycoconjugatesGlycolipidsMiceMice, TransgenicAzoxymethaneDextransGangliosidesGlycoconjugatesGlycolipidsNeu3 protein, mouseNeuraminidaseSialic Acidssodium sulfateSulfates

Identifiers

PMID22815940
PMCPMC3398939
OpenAlexW2052544294

What OpenQuestion holds

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LicenceCC BY
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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.