Evidence map›Paper›PMID 26730334›Full record

ArticleIranian journal of basic medical sciences2015

CuO nanoparticles induce cytotoxicity and apoptosis in human K562 cancer cell line via mitochondrial pathway, through reactive oxygen species and P53.

Maryam Shafagh, Fatemeh Rahmani, Norouz Delirezh

Abstract read
In one paragraph

Article in Iranian journal of basic medical sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

52 citing papers in PubMed, 127 citations in OpenAlex.

  1. Review
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  9. Article
  10. Involvement of copper in cell death and cancer.Apoptosis : an international journal on programmed cell death · 2025
    Review
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  12. Analyzing antibacterial potential of bellamyaFrontiers in pharmacology · 2025
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  13. Rapid synthesis of highly monodisperse AgSbSBeilstein journal of nanotechnology · 2025
    Article
  14. Article
  15. Article
  16. Review
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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

3 authors at 1 institution in 1 country.

Maryam ShafaghDepartment of Biology and Institute of Biotechnology, Faculty of Sciences, Urmia University, Urmia, Iran.
Fatemeh RahmaniDepartment of Biology and Institute of Biotechnology, Faculty of Sciences, Urmia University, Urmia, Iran.
Norouz DelirezhMicrobiology Department, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran.
Urmia University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThis study focused on determining cytotoxic effects of copper oxide nanoparticles (CuO NPs) on chronic myeloid leukemia (CML) K562 cell line in a cell-specific manner and its possible mechanism of cell death. We investigated the cytotoxicity of CuO NPs against K562 cell line (cancerous cell) and peripheral blood mononuclear cell (normal cell). MATERIALS AND

methodsThe toxicity was evaluated using cell viability, oxidative stress and apoptosis detection. In addition, the expression levels of P53, Caspase 3, Bcl-2, and Bax genes in K562 cells were studied by reverse transcription polymerase chain reaction (RT-PCR) analysis.

resultsCuO NPs exerted distinct effects on cell viability via selective killing of cancer cells in a dose-dependent manner while not impacting normal cells in MTT assay. The dose-dependent cytotoxicity of CuO NPs against K562 cells was shown through reactive oxygen species (ROS) generation. The CuO NPs induced apoptosis was confirmed through acridine orange and propidium iodide double staining. Tumor suppressor gene P53 was up regulated due to CuO NPs exposure, and increase in Bax/Bcl-2 ratio suggested mitochondria-mediated pathway is involved in CuO NPs induced apoptosis. We also observed that Caspase 3 gene expression remained unchanged up to 24 hr exposure.

conclusionThese molecular alterations provide an insight into CuO NPs-caused inhibition of growth, generation of ROS, and apoptotic death of K562 cells.

Indexed as

ApoptosisBax/Bcl-2CuO NPsK562P53ROS

Identifiers

PMID26730334
PMCPMC4686584
OpenAlexW2212304484

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.