Evidence map›Paper›PMID 24253505›Full record

ArticleBritish journal of cancer2014

Fucosylated TGF-β receptors transduces a signal for epithelial-mesenchymal transition in colorectal cancer cells.

M Hirakawa, R Takimoto, F Tamura, M Yoshida, M Ono, K Murase, Y Sato, T Osuga, T Sato, S Iyama and 5 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

62 citing papers in PubMed, 94 citations in OpenAlex.

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  19. Nomograms Based on SerumCurrent oncology (Toronto, Ont.) · 2022
    Article
  20. High expression ofThe Indian journal of medical research · 2022
    Article

2 more citing papers are in PubMed but not listed here.

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

15 authors at 1 institution in 1 country.

M Hirakawa1] Department of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan [2] Division of Clinical Oncology, Sapporo Medical University Graduate School of Medicine, Sapporo, Japan.
R Takimoto1] Department of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan [2] Division of Clinical Oncology, Sapporo Medical University Graduate School of Medicine, Sapporo, Japan.
F Tamura1] Department of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan [2] Division of Clinical Oncology, Sapporo Medical University Graduate School of Medicine, Sapporo, Japan.
M Yoshida1] Department of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan [2] Division of Clinical Oncology, Sapporo Medical University Graduate School of Medicine, Sapporo, Japan.
M Ono1] Department of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan [2] Division of Clinical Oncology, Sapporo Medical University Graduate School of Medicine, Sapporo, Japan.
K MuraseDepartment of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Y SatoDepartment of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan.
T OsugaDepartment of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan.
T Sato1] Department of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan [2] Division of Molecular Oncology, Sapporo Medical University Graduate School of Medicine, Sapporo, Japan.
S IyamaDepartment of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan.
K MiyanishiDepartment of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan.
K TakadaDepartment of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan.
T HayashiDepartment of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan.
M KobuneDivision of Molecular Oncology, Sapporo Medical University Graduate School of Medicine, Sapporo, Japan.
J Kato1] Department of Medical Oncology and Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan [2] Division of Clinical Oncology, Sapporo Medical University Graduate School of Medicine, Sapporo, Japan.
Sapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTransforming growth factor-β (TGF-β) is a major inducer of epithelial-mesenchymal transition (EMT) in different cell types. TGF-β-mediated EMT is thought to contribute to tumour cell spread and metastasis. Sialyl Lewis antigens synthesised by fucosyltransferase (FUT) 3 and FUT6 are highly expressed in patients with metastatic colorectal cancer (CRC) and are utilised as tumour markers for cancer detection and evaluation of treatment efficacy. However, the role of FUT3 and FUT6 in augmenting the malignant potential of CRC induced by TGF-β is unclear.

methodsColorectal cancer cell lines were transfected with siRNAs for FUT3/6 and were examined by cell proliferation, invasion and migration assays. The expression and phosphorylation status of TGF-β downstream molecules were analysed by western blot. Fucosylation of TGF-β receptor (TβR) was examined by lectin blot analysis.

resultsInhibition of FUT3/6 expression by siRNAs suppressed the fucosylation of type I TβR and phosphorylation of the downstream molecules, thereby inhibiting the invasion and migration of CRC cells by EMT.

conclusionFucosyltransferase 3/6 has an essential role in cancer cell adhesion to endothelial cells by upregulation of sialyl Lewis antigens and also by enhancement of cancer cell migration through TGF-β-mediated EMT.

Indexed as

Cell AdhesionCell Line, TumorColorectal NeoplasmsEpithelial-Mesenchymal TransitionFucosyltransferasesHT29 CellsHumansPhosphorylationReceptors, Transforming Growth Factor betaRNA, Small InterferingSignal TransductionSmad ProteinsTransfectionTransforming Growth Factor betaUp-Regulation3-galactosyl-N-acetylglucosaminide 4-alpha-L-fucosyltransferaseFucosyltransferasesFUT6 protein, humanReceptors, Transforming Growth Factor betaRNA, Small InterferingSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID24253505
PMCPMC3887298
OpenAlexW2039553809

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.