Evidence map›Paper›PMID 27119350›Full record

ArticleOncotarget2016

Interference with mutagenic aflatoxin B1-induced checkpoints through antagonistic action of ochratoxin A in intestinal cancer cells: a molecular explanation on potential risk of crosstalk between carcinogens.

Juil Kim, Seong-Hwan Park, Kee Hun Do, Dongwook Kim, Yuseok Moon

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
7.5field-weighted citation impact, top 4% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Article
  7. Review
  8. Review
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  11. Review
  12. Aflatoxin BFrontiers in immunology · 2018
    Article
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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 3 institutions in 1 country.

Juil KimLaboratory of Mucosal Exposome and Biomodulation, Department of Biomedical Sciences and Medical Research Institute, Pusan National University School of Medicine, Yangsan, South Korea.
Seong-Hwan ParkLaboratory of Mucosal Exposome and Biomodulation, Department of Biomedical Sciences and Medical Research Institute, Pusan National University School of Medicine, Yangsan, South Korea.
Kee Hun DoLaboratory of Mucosal Exposome and Biomodulation, Department of Biomedical Sciences and Medical Research Institute, Pusan National University School of Medicine, Yangsan, South Korea.
Dongwook KimNational Institute of Animal Science, RDA, Wanju, South Korea.
Yuseok MoonLaboratory of Mucosal Exposome and Biomodulation, Department of Biomedical Sciences and Medical Research Institute, Pusan National University School of Medicine, Yangsan, South Korea.
Pusan National University · KRInstitute for Basic Science · KRNational Institute of Animal Science · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Foodborne aflatoxin B1 (AFB1) and ochratoxin A (OTA) cause genotoxic injury and subsequent tumor formation. As a biomarker of oncogenic stimulation by genotoxic mycotoxins, p53-triggered Mdm2 was assessed in intestinal cancer cells. AFB1 increased Mdm2 reporter expression in a dose-dependent manner. However, this was strongly antagonized by OTA treatment. As a positive transcription factor of Mdm2 expression, p53 levels were also increased by AFB1 alone and reduced by OTA. With marginal cell death responses, AFB1 induced p53-mediated S phase arrest and cell cycle-regulating target genes, which was completely suppressed by OTA. Although enterocyte-dominant CYP3A5 counteracted AFB1-induced DNA damage, expression of CYP3A5 was decreased by OTA or AFB1. Instead, OTA enhanced expression of another metabolic inactivating enzyme CYP3A4, attenuation of formation of AFB1-DNA adduct and p53-mediated cell cycle checking responses to the mutagens. Finally, the growth of intestinal cancer cells exposed to the mycotoxin mixture significantly exceeded the expected growth calculated from that of cells treated with each mycotoxin. Although AFB1-induced mutagen formation was decreased by OTA, interference with checkpoints through antagonistic action of OTA may contribute to the survival of tumor cells with deleterious mutations by genotoxic mycotoxins, potently increasing the risk of carcinogenesis.

Indexed as

Drug InteractionsMutagensAflatoxin B1CarcinogensCell Cycle CheckpointsCell Line, TumorCell SeparationCytochrome P-450 CYP3ADNA AdductsDNA DamageDose-Response Relationship, DrugFlow CytometryGenomeHCT116 CellsHumansIntestinal NeoplasmsAflatoxin B1CarcinogensCYP3A5 protein, humanCytochrome P-450 CYP3ADNA AdductsMDM2 protein, humanMutagensochratoxin AOchratoxinsProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53aflatoxinintestinal cancer cellsMdm2 proteinochratoxinp53 protein

Identifiers

PMID27119350
PMCPMC5129958
OpenAlexW2338475115

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.