Evidence map›Paper›PMID 24662817›Full record

ArticleOncogene2015

Integrated genomic and functional analyses reveal glyoxalase I as a novel metabolic oncogene in human gastric cancer.

F Hosoda, Y Arai, N Okada, H Shimizu, M Miyamoto, N Kitagawa, H Katai, H Taniguchi, K Yanagihara, I Imoto and 3 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Dual roles of methylglyoxal in cancer.Frontiers in oncology · 2025
    Review
  3. Computational fragment-based drug design of potential Glo-I inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2024
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Identification of HAGHL as a novel metabolic oncogene regulating human colorectal cancer progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Glyoxalase System in the Progression of Skin Aging and Skin Malignancies.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Article
  18. Article
  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

13 authors at 3 institutions in 1 country.

F HosodaDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
Y AraiDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
N OkadaDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
H ShimizuDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
M MiyamotoDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
N KitagawaDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
H KataiDivision of Gastric Surgery, National Cancer Center Hospital, Tokyo, Japan.
H TaniguchiDivision of Clinical Laboratory, National Cancer Center Hospital, Tokyo, Japan.
K YanagiharaDivision of Translational Research, Exploratory Oncology Research & Clinical Trial Center, National Cancer Center, Chiba, Japan.
I Imoto1] Department of Molecular Cytogenetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan [2] Department of Human Genetics and Public Health, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.
J InazawaDepartment of Molecular Cytogenetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
M OhkiDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
T ShibataDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
Tokyo Medical and Dental University · JPTokyo National Hospital · JPChiba Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosomal abnormalities are good guideposts when hunting for cancer-related genes. We analyzed copy number alterations of 163 primary gastric cancers using array-based comparative genomic hybridization and simultaneously performed a genome-wide integrated analysis of copy number and gene expression using microarray data for 58 tumors. We showed that chromosome 6p21 amplification frequently occurred secondary to ERBB2 amplification, was associated with poorer prognosis and caused overexpression of half of the genes mapped. A comprehensive small interfering RNA knockdown of 58 genes overexpressed in tumors identified 32 genes that reduced gastric cancer cell growth. Enforced expression of 16 of these genes promoted cell growth in vitro, and six genes showing more than two-fold activity conferred tumor-forming ability in vivo. Among these six candidates, GLO1, encoding a detoxifying enzyme glyoxalase I (GLO1), exhibited the strongest tumor-forming activity. Coexpression of other genes with GLO1 enhanced growth-stimulating activity. A GLO1 inhibitor, S-p-bromobenzyl glutathione cyclopentyl diester, inhibited the growth of two-thirds of 24 gastric cancer cell lines examined. The efficacy was found to be associated with the mRNA expression ratio of GLO1 to GLO2, encoding glyoxalase II (GLO2), another constituent of the glyoxalase system. GLO1 downregulation affected cell growth through inactivating central carbon metabolism and reduced the transcriptional activities of nuclear factor kappa B and activator protein-1. Our study demonstrates that GLO1 is a novel metabolic oncogene of the 6p21 amplicon, which promotes tumor growth and aberrant transcriptional signals via regulating cellular metabolic activities for energy production and could be a potential therapeutic target in gastric cancer.

Indexed as

AnimalsCell Line, TumorChromosomes, Human, Pair 6Comparative Genomic HybridizationErb-b2 Receptor Tyrosine KinasesGene AmplificationGene DosageGenomicsGlutathioneHEK293 CellsHumansLactoylglutathione LyaseMiceNF-kappa BNIH 3T3 CellsSignal TransductionERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesGlutathioneLactoylglutathione LyaseNF-kappa BS-4-bromobenzylglutathione cyclopentyl diesterTranscription Factor AP-1

Identifiers

PMID24662817
OpenAlexW2029236582

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.