Evidence map›Paper›PMID 24903013›Full record

ArticleCancer gene therapy2014

Enhanced expression of the β4-galactosyltransferase 2 gene impairs mammalian tumor growth.

M Tagawa, K Shirane, L Yu, T Sato, S Furukawa, H Mizuguchi, R Kuji, K Kawamura, N Takahashi, K Kato and 3 more

Open access · bronzeAbstract read
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In one paragraph

Article in Cancer gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Challenge to the suppression of tumor growth by the β4-galactosyltransferase genes.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2015
    Review
  3. 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

13 authors at 6 institutions in 1 country.

M Tagawa1] Division of Pathology and Cell Therapy, Chiba Cancer Research Institute, Chiba, Chiba, Japan [2] Department of Molecular Biology and Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
K ShiraneDepartment of Biosignal Research, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
L YuDivision of Pathology and Cell Therapy, Chiba Cancer Research Institute, Chiba, Chiba, Japan.
T Sato1] Department of Biosignal Research, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan [2] Laboratory of Glycobiology, Department of Bioengineering, Nagaoka University of Technology, Nagaoka, Japan.
S FurukawaLaboratory of Molecular and Genetic Information, Institute of Molecular and Cellular Biosciences, the University of Tokyo, Tokyo, Japan.
H MizuguchiLaboratory of Biochemistry and Molecular Biology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
R KujiLaboratory of Glycobiology, Department of Bioengineering, Nagaoka University of Technology, Nagaoka, Japan.
K KawamuraDivision of Pathology and Cell Therapy, Chiba Cancer Research Institute, Chiba, Chiba, Japan.
N TakahashiGraduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
K Kato1] Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan [2] Okazaki Institute for Integrative Bioscience and Institute for Molecular Science, National Institutes of Natural Sciences, Okazaki, Japan.
S HayakawaDepartment of Biosignal Research, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
S Sawada1] Department of Biosignal Research, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan [2] Laboratory of Glycobiology, Department of Bioengineering, Nagaoka University of Technology, Nagaoka, Japan.
K Furukawa1] Department of Biosignal Research, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan [2] Laboratory of Glycobiology, Department of Bioengineering, Nagaoka University of Technology, Nagaoka, Japan.
Chiba Cancer Center · JPNagaoka University of Technology · JPTokyo Metropolitan Institute of Gerontology · JPNagoya City University · JPOsaka University of Pharmaceutical Sciences · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered N-glycosylation of membrane proteins is associated with malignant transformation of cells. We found that the expression of the β4-galactosyltransferase 2 (β4GalT2) gene is decreased markedly during the transformation. Here, we examined whether the tumor growth activity of B16-F10 mouse melanoma cells can be reduced by the enhanced expression of the β4GalT2 gene. We isolated a clone, B16-β4GalT2, showing its β4GalT2 transcript 2.5 times higher than a control clone, B16-mock, by transducing its cDNA, and transplanted them subcutaneously into C57BL/6 mice to examine their tumor growth activity. The results showed that the average size of tumors formed with B16-mock cells is 13.1±0.76 mm, whereas that of tumors formed with B16-β4GalT2 cells is 5.1±1.13 mm (P<0.01) 2 weeks after transplantation. Immunohistochemical analyses showed that the apoptosis and the suppression of angiogenesis are induced in the tumors upon transduction of the β4GalT2 gene. To pursue a clinical usefulness of the β4GalT2 gene for suppressing human tumor growth, we injected adenoviruses carrying the human β4GalT2 cDNA into HuH-7 human hepatocellular carcinomas developed in severe combined immunodeficient mice, and observed marked growth retardation of the tumors. The enhancement of the β4GalT2 gene expression in tumors is one of the promising approaches to suppress human tumor growth.

Indexed as

AnimalsCell ProliferationFemaleGalactosyltransferasesGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMelanoma, ExperimentalMembrane ProteinsMice, Inbred BALB CMice, Inbred C57BLMice, SCIDTransduction, Geneticbeta-1,4-galactosyltransferase IIGalactosyltransferasesMembrane Proteins

Identifiers

PMID24903013
OpenAlexW2045689109

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.