Evidence map›Paper›PMID 24261884›Full record

ArticleBMC cancer2013

Glutamate acid decarboxylase 1 promotes metastasis of human oral cancer by β-catenin translocation and MMP7 activation.

Ryota Kimura, Atsushi Kasamatsu, Tomoyoshi Koyama, Chonji Fukumoto, Yukinao Kouzu, Morihiro Higo, Yosuke Endo-Sakamoto, Katsunori Ogawara, Masashi Shiiba, Hideki Tanzawa and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

38 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Cloning, expression, purification, and characterization of glutamate decarboxylase (Rv3432c) from Mycobacterium tuberculosis.International microbiology : the official journal of the Spanish Society for Microbiology · 2025
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
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  14. Cooperative Interaction between Acid and Copper Resistance inJournal of microbiology and biotechnology · 2022
    Article
  15. Insight into the Role of Psychological Factors in Oral Mucosa Diseases.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Bridging the Metabolic Parallels Between Neurological Diseases and Cancer.Advances in experimental medicine and biology · 2021
    Article
  20. Review
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

11 authors at 2 institutions in 1 country.

Ryota Kimura
Atsushi KasamatsuDepartment of Clinical Molecular Biology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan. kasamatsua@faculty.chiba-u.jp.
Tomoyoshi Koyama
Chonji Fukumoto
Yukinao Kouzu
Morihiro Higo
Yosuke Endo-Sakamoto
Katsunori Ogawara
Masashi Shiiba
Hideki Tanzawa
Katsuhiro Uzawa
Chiba University · JPChiba University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlutamate decarboxylase 1 (GAD1), a rate-limiting enzyme in the production of γ-aminobutyric acid (GABA), is found in the GABAergic neurons of the central nervous system. Little is known about the relevance of GAD1 to oral squamous cell carcinoma (OSCC). We investigated the expression status of GAD1 and its functional mechanisms in OSCCs.

methodsWe evaluated GAD1 mRNA and protein expressions in OSCC-derived cells using real-time quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and immunoblotting analyses. To assess the critical functions of GAD1, i.e., cellular proliferation, invasiveness, and migration, OSCC-derived cells were treated with the shRNA and specific GAD1 inhibitor, 3-mercaptopropionic acid (3-MPA). GAD1 expression in 80 patients with primary OSCCs was analyzed and compared to the clinicopathological behaviors of OSCC.

resultsqRT-PCR and immunoblotting analyses detected frequent up-regulation of GAD1 in OSCC-derived cells compared to human normal oral keratinocytes. Suppression of nuclear localization of β-catenin and MMP7 secretion was observed in GAD1 knockdown and 3-MPA-treated cells. We also found low cellular invasiveness and migratory abilities in GAD1 knockdown and 3-MPA-treated cells. In the clinical samples, GAD1 expression in the primary OSCCs was significantly (P < 0.05) higher than in normal counterparts and was correlated significantly (P < 0.05) with regional lymph node metastasis.

conclusionsOur data showed that up-regulation of GAD1 was a characteristic event in OSCCs and that GAD1 was correlated with cellular invasiveness and migration by regulating β-catenin translocation and MMP7 activation. GAD1 might play an important role in controlling tumoral invasiveness and metastasis in oral cancer.

Indexed as

3-Mercaptopropionic AcidAdultAgedAged, 80 and overbeta CateninCarcinoma, Squamous CellCell Line, TumorCell MovementCell NucleusCell ProliferationEnzyme ActivationGlutamate DecarboxylaseHumansMatrix Metalloproteinase 7Middle AgedMouth Neoplasms3-Mercaptopropionic Acidbeta CateninCTNNB1 protein, humanGlutamate Decarboxylaseglutamate decarboxylase 1Matrix Metalloproteinase 7MMP7 protein, human

Identifiers

PMID24261884
PMCPMC3866561
OpenAlexW2115709937

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.