Evidence map›Paper›PMID 24504364›Full record

ArticleBritish journal of cancer2014

DJ-1 upregulates breast cancer cell invasion by repressing KLF17 expression.

I A Ismail, H S Kang, H-J Lee, J-K Kim, S-H Hong

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 50 citations in OpenAlex.

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  14. Towards Discovery and Targeted Peptide Biomarker Detection Using nanoESI-TIMS-TOF MS.Journal of the American Society for Mass Spectrometry · 2018
    Article
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  19. DJ-1 Expression in Cervical Carcinoma and its Effects on Cell Viability and Apoptosis.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  20. Krüppel-like factor 17, a novel tumor suppressor: its low expression is involved in cancer metastasis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

5 authors at 2 institutions in 2 countries.

I A Ismail1] Department of Oral Microbiology, School of Dentistry, Kyungpook National University, Daegu 700-412, Republic of Korea [2] Laboratory of Molecular Cell Biology, Department of Zoology, Faculty of Science, Assiut University, Assiut 71516, Egypt.
H S KangDepartment of Oral Microbiology, School of Dentistry, Kyungpook National University, Daegu 700-412, Republic of Korea.
H-J LeeDepartment of Oral Microbiology, School of Dentistry, Kyungpook National University, Daegu 700-412, Republic of Korea.
J-K KimDepartment of Oral Microbiology, School of Dentistry, Kyungpook National University, Daegu 700-412, Republic of Korea.
S-H HongDepartment of Oral Microbiology, School of Dentistry, Kyungpook National University, Daegu 700-412, Republic of Korea.
Kyungpook National University · KRAssiut University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDJ-1 (PARK7) was reported as an oncogene in a Ras-dependent manner. Recent studies have shown that DJ-1 stimulates cell proliferation, cell invasion, and cancer metastasis. However, the molecular mehchanism by which DJ-1 induces cancer cell invasion and metastasis remains unclear.

methodsBreast cancer cells were transfected with DJ-1 siRNA or DJ-1 overexpression to investigate the effect of DJ-1 on KLF17 expression. ID-1 luciferase promoter assay was performed to evaluate DJ-1-dependent KLF17 expression changes. In addition, Epistasis analysis of DJ-1 and KLF17 was performed to evaluate their regulatory interactions. Ras inhibitors were pretreated to determine whether DJ-1 regulates cell invasion in a Ras-dependent manner.

resultsI n the present study, we found increased DJ-1 expression in highly invasive breast cancer cells as compared with non-metastatic cells. Furthermore, DJ-1 promoted breast cancer cell invasion by downregulating E-cadherin and increasing Snail expression. Interestingly, exogenous DJ-1 overexpression markedly decreased mRNA and protein expression of KLF17, the EMT negative regulator. These data were confirmed by ID-1 promoter activity, which is directly regulated by DJ-1-dependent KLF17 transcription factor. Epistasis analysis showed that KLF17 overexpression overcomes increased cell invasion by DJ-1, suggesting that KLF17 might be one of the downstream signalling molecules of DJ-1. Acceleration of cell invasion by DJ-1 was alleviated by Ras inhibitors, suggesting that DJ-1 cooperates with Ras to increase cell invasion.

conclusionAltogether, these data suggest for the first time that DJ-1 acts as an EMT-positive regulator in breast cancer cells via regulation of the KLF17/ID-1 pathway.

Indexed as

Breast NeoplasmsCell Line, TumorDown-RegulationFemaleHumansIntracellular Signaling Peptides and ProteinsMCF-7 CellsNeoplasm InvasivenessOncogene ProteinsPromoter Regions, GeneticProtein Deglycase DJ-1Transcription FactorsUp-RegulationIntracellular Signaling Peptides and ProteinsKLF17 protein, humanOncogene ProteinsPARK7 protein, humanProtein Deglycase DJ-1Transcription Factors

Identifiers

PMID24504364
PMCPMC3950878
OpenAlexW2062901537

What OpenQuestion holds

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LicenceCC BY-NC-SA
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Registered trials

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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.