Evidence map›Paper›PMID 18808525›Full record

ArticleInternational journal of experimental pathology2008

A role of fukutin, a gene responsible for Fukuyama type congenital muscular dystrophy, in cancer cells: a possible role to suppress cell proliferation.

Tomoko Yamamoto, Yoichiro Kato, Noriyuki Shibata, Tatsuo Sawada, Makiko Osawa, Makio Kobayashi

Open access · greenAbstract read
In one paragraph

Article in International journal of experimental pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Fukutin regulates tau phosphorylation and synaptic function: Novel properties of fukutin in neurons.Neuropathology : official journal of the Japanese Society of Neuropathology · 2022
    Article
  5. Article
  6. Article
  7. Fukutin, identified by the Escherichia coli ampicillin secretion trap (CAST) method, participates in tumor progression in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2016
    Article
  8. Article
  9. Post-transcriptional regulation of fukutin in an astrocytoma cell line.International journal of experimental pathology · 2012
    Article
  10. Article
  11. Article
  12. Congenital Muscular Dystrophy due toAnnals of Indian Academy of Neurology
    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

6 authors at 1 institution in 1 country.

Tomoko YamamotoDepartment of Pathology, Tokyo Women's Medical University, Shinjuku-ku, Tokyo, Japan. sheto@research.twmu.ac.jp
Yoichiro Kato
Noriyuki Shibata
Tatsuo Sawada
Makiko Osawa
Makio Kobayashi
Tokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fukutin, a gene responsible for Fukuyama type congenital muscular dystrophy (FCMD), is presumably related to the glycosylation of alpha-dystroglycan (alpha-DG), involved in basement membrane formation. Hypoglycosylation of alpha-DG plays a key role for the pathogenesis of FCMD. On the other hand, fukutin and alpha-DG are also expressed in various non-neuromuscular tissues. Recently, a role of alpha-DG as a cancer suppressor has been proposed, because of a decrease of glycosylated alpha-DG in cancers. In this study, function of fukutin was investigated in two cancer cell lines, focusing on whether fukutin is involved in the glycosylation of alpha-DG in cancer cells and has any possible roles related to a cancer suppressor. Localization of fukutin and a result of laminin-binding assay after RNA interference suggest that fukutin may be involved in the glycosylation of alpha-DG in a small portion in these cancer cell lines. In Western blotting and immuno-electron microscopy, localization of fukutin in the nucleus was suggested in addition to the Golgi apparatus and/or endoplasmic reticulum. Immunohistochemically, there were more Ki-67-positive cells and more nuclear staining of phosphorylated c-jun after knockdown of fukutin in two cell lines. Fukutin appears to suppress cell proliferation through a system involving c-jun, although it is unclear this process is related to alpha-DG or not at present. The result may propose a possibility of another function of fukutin in addition to the glycosylation of alpha-DG in cancer cells.

Indexed as

Blotting, WesternBreast NeoplasmsCell Line, TumorCell NucleusCell ProliferationDystroglycansGlycosylationHeLa CellsHumansMembrane ProteinsMicroscopy, ImmunoelectronMuscular DystrophiesRNA InterferenceRNA, Small InterferingDystroglycansFKTN protein, humanMembrane ProteinsRNA, Small Interfering

Identifiers

PMID18808525
PMCPMC2613979
OpenAlexW1585188701

What OpenQuestion holds

Textmetadata
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.