Evidence map›Paper›PMID 26339654›Full record

ArticleBioMed research international2015

Impact of Cadmium on Intracellular Zinc Levels in HepG2 Cells: Quantitative Evaluations and Molecular Effects.

Chiara Urani, Pasquale Melchioretto, Maurizio Bruschi, Marco Fabbri, Maria Grazia Sacco, Laura Gribaldo

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 16% 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, 37 citations in OpenAlex.

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  10. In vitro and bioinformatics mechanistic-based approach for cadmium carcinogenicity understanding.Toxicology in vitro : an international journal published in association with BIBRA · 2020
    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

6 authors at 3 institutions in 1 country.

Chiara UraniDepartment of Earth and Environmental Sciences, University of Milan Bicocca, Piazza della Scienza 1, 20126 Milan, Italy.
Pasquale MelchiorettoDepartment of Earth and Environmental Sciences, University of Milan Bicocca, Piazza della Scienza 1, 20126 Milan, Italy.
Maurizio BruschiDepartment of Earth and Environmental Sciences, University of Milan Bicocca, Piazza della Scienza 1, 20126 Milan, Italy.
Marco FabbriDepartment of Clinical and Experimental Medicine, University of Insubria, 21100 Varese, Italy.
Maria Grazia SaccoMolecular Biology and Genomics Unit, Institute for Health and Consumer Protection, DG JRC, European Commission, Via Enrico Fermi 2749, 21027 Ispra, Italy.
Laura GribaldoChemical Assessment and Testing Unit (CAT), Institute for Health and Consumer Protection, DG JRC, European Commission, Via Enrico Fermi 2749, 21027 Ispra, Italy.
University of Milano-Bicocca · ITJoint Research Centre · ITUniversity of Insubria · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cadmium is classified as a human carcinogen, and its disturbance in zinc homeostasis has been well established. However, its extent as well as molecular mechanisms involved in cadmium carcinogenesis has yet to be fully clarified. To this end, we used the zinc specific probe Zinquin to visualize and to quantitatively evaluate changes in the concentration of labile zinc, in an in vitro model of human hepatic cells (HepG2) exposed to cadmium. A very large increase (+93%) of intracellular labile zinc, displaced by cadmium from the zinc proteome, was measured when HepG2 were exposed to 10 µM cadmium for 24 hrs. Microarray expression profiling showed that in cells, featuring an increase of labile zinc after cadmium exposure, one of the top regulated genes is Snail1 (+3.6), which is included in the adherens junction pathway and linked to cancer. In the same pathway MET, TGF-βR, and two members of the Rho-family GTPase, Rac, and cdc42 all implicated in the loss of adherence features and acquisition of migratory and cancer properties were regulated, as well. The microRNAs analysis showed a downregulation of miR-34a and miR-200a, both implicated in the epithelial-mesenchymal transition. These microRNAs results support the role played by zinc in affecting gene expression at the posttranscriptional level.

Indexed as

CadmiumCarcinogenesisCytoplasmEpithelial-Mesenchymal TransitionGene Expression ProfilingGene Expression Regulation, NeoplasticHep G2 CellsHumansMicroRNAsSnail Family Transcription FactorsTranscription FactorsZincCadmiumMicroRNAsMIRN200 microRNA, humanMIRN34 microRNA, humanSNAI1 protein, humanSnail Family Transcription FactorsTranscription FactorsZinc

Identifiers

PMID26339654
PMCPMC4538774
OpenAlexW1494412517

What OpenQuestion holds

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LicenceCC BY
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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.