Evidence map›Paper›PMID 27291325›Full record

ArticleScientific reports2016

Silver nanoparticles defeat p53-positive and p53-negative osteosarcoma cells by triggering mitochondrial stress and apoptosis.

Dávid Kovács, Nóra Igaz, Csilla Keskeny, Péter Bélteky, Tímea Tóth, Renáta Gáspár, Dániel Madarász, Zsolt Rázga, Zoltán Kónya, Imre M Boros and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 119 citations in OpenAlex.

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  17. Cancer Therapy by Silver Nanoparticles: Fiction or Reality?International journal of molecular sciences · 2022
    Review
  18. Review
  19. Nano Silver-Induced Toxicity and Associated Mechanisms.International journal of nanomedicine · 2022
    Review
  20. Silver Nanoparticles Derived byInternational journal of molecular sciences · 2021
    Article
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.

Dávid KovácsDepartment of Biochemistry and Molecular Biology, University of Szeged, Középfasor 52, H-6726, Szeged, Hungary.
Nóra IgazDepartment of Biochemistry and Molecular Biology, University of Szeged, Középfasor 52, H-6726, Szeged, Hungary.
Csilla KeskenyDepartment of Biochemistry and Molecular Biology, University of Szeged, Középfasor 52, H-6726, Szeged, Hungary.
Péter BéltekyDepartment of Applied and Environmental Chemistry, University of Szeged, Rerrich Béla tér 1. H-6720, Szeged, Hungary.
Tímea TóthDepartment of Applied and Environmental Chemistry, University of Szeged, Rerrich Béla tér 1. H-6720, Szeged, Hungary.
Renáta GáspárDepartment of Biochemistry, Faculty of Medicine, University of Szeged, Dóm tér 9. Szeged, H-6720, Hungary.
Dániel MadarászDepartment of Applied and Environmental Chemistry, University of Szeged, Rerrich Béla tér 1. H-6720, Szeged, Hungary.
Zsolt RázgaDepartment of Pathology, University of Szeged, Állomás utca. 2. H-6720, Szeged, Hungary.
Zoltán KónyaDepartment of Applied and Environmental Chemistry, University of Szeged, Rerrich Béla tér 1. H-6720, Szeged, Hungary.
Imre M BorosDepartment of Biochemistry and Molecular Biology, University of Szeged, Középfasor 52, H-6726, Szeged, Hungary.
Mónika KiricsiDepartment of Biochemistry and Molecular Biology, University of Szeged, Középfasor 52, H-6726, Szeged, Hungary.
University of Szeged · HUHUN-REN Szegedi Biológiai Kutatóközpont · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of function of the tumour suppressor p53 observed frequently in human cancers challenges the drug-induced apoptotic elimination of cancer cells from the body. This phenomenon is a major concern and provides much of the impetus for current attempts to develop a new generation of anticancer drugs capable of provoking apoptosis in a p53-independent manner. Since silver nanoparticles (AgNPs) possess unique cytotoxic features, we examined, whether their activity could be exploited to kill tumour suppressor-deficient cancer cells. Therefore, we investigated the effects of AgNPs on osteosarcoma cells of different p53 genetic backgrounds. As particle diameters might influence the molecular mechanisms leading to AgNP-induced cell death we applied 5 nm and 35 nm sized citrate-coated AgNPs. We found that both sized AgNPs targeted mitochondria and induced apoptosis in wild-type p53-containing U2Os and p53-deficient Saos-2 cells. According to our findings AgNPs are able to kill osteosarcoma cells independently from their actual p53 status and induce p53-independent cancer cell apoptosis. This feature renders AgNPs attractive candidates for novel chemotherapeutic approaches.

Indexed as

ApoptosisBone NeoplasmsCell Line, TumorCitric AcidHumansMembrane Potential, MitochondrialMetal NanoparticlesMicroscopy, ConfocalMicroscopy, Electron, TransmissionMitochondriaOsteosarcomaParticle SizeSignal TransductionSilverTumor Suppressor Protein p53Citric AcidSilverTumor Suppressor Protein p53

Identifiers

PMID27291325
PMCPMC4904210
OpenAlexW2437719412

What OpenQuestion holds

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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.