Evidence map›Paper›PMID 25101185›Full record

ArticleISRN toxicology2014

Cadmium Impairs p53 Activity in HepG2 Cells.

C Urani, P Melchioretto, M Fabbri, G Bowe, E Maserati, L Gribaldo

Open access · diamondAbstract read
In one paragraph

Article in ISRN toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 41 citations in OpenAlex.

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  8. Cell Viability and Immune Response to Low Concentrations of Nickel and Cadmium: An In Vitro Model.International journal of environmental research and public health · 2020
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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.

C UraniDepartment of Earth and Environmental Sciences, University of Milano Bicocca, piazza della Scienza 1, 20126 Milan, Italy.
P MelchiorettoDepartment of Earth and Environmental Sciences, University of Milano Bicocca, piazza della Scienza 1, 20126 Milan, Italy.
M FabbriInstitute for Health and Consumer Protection, Joint Research Centre, Via Enrico Fermi 2749, 21027 Ispra, Italy ; Dipartimento di Medicina Clinica e Sperimentale, Università dell'Insubria, 21100 Varese, Italy.
G BoweInstitute for Health and Consumer Protection, Joint Research Centre, Via Enrico Fermi 2749, 21027 Ispra, Italy.
E MaseratiDipartimento di Medicina Clinica e Sperimentale, Università dell'Insubria, 21100 Varese, Italy.
L GribaldoInstitute for Health and Consumer Protection, Joint Research Centre, Via Enrico Fermi 2749, 21027 Ispra, Italy.
Joint Research Centre · ITUniversity of Milano-Bicocca · ITUniversity of Insubria · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cadmium and cadmium compounds are contaminants of the environment, food, and drinking water and are important constituents of cigarette smoke. Cd exposure has also been associated with airborne particulate CdO and with Cd-containing quantum dots in medical therapy. Adverse cadmium effects reported in the literature have stimulated during recent years an ongoing discussion to better elucidate cadmium outcomes at cell and molecular level. The present work is designed to gain an insight into the mechanism of p53 impairment at gene and protein level to understand Cd-induced resistance to apoptosis. We used a hepatoma cell line (HepG2) derived from liver, known to be metal responsive. At genotoxic cadmium concentrations no cell cycle arrest was observed. The p53 at gene and protein level was not regulated. Fluorescence images showed that p53 was correctly translocated into the nucleus but that the p21(Cip1/WAF-1), a downstream protein of p53 network involved in cell cycle regulation, was not activated at the highest cadmium concentrations used. The miRNAs analysis revealed an upregulation of mir-372, an miRNA able to affect p21(Cip1/WAF-1) expression and promote cell cycle progression and proliferation. The role of metallothioneins and possible conformational changes of p53 are discussed.

Identifiers

PMID25101185
PMCPMC3976861
OpenAlexW2029869662

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.