Evidence map›Paper›PMID 29214213›Full record

ArticleAnnals of clinical pathology2017

Therapeutic Potential of Arsenic Trioxide (ATO) in Treatment of Hepatocellular Carcinoma: Role of Oxidative Stress in ATO-Induced Apoptosis.

Erika B Dugo, Clement G Yedjou, Jacqueline J Stevens, Paul B Tchounwou

Open access · greenAbstract read
In one paragraph

Article in Annals of clinical pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

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  8. Effect of lycopene on AsMolecular biology reports · 2021
    Article
  9. Targeting Redox Metabolism in Pancreatic Cancer.International journal of molecular sciences · 2021
    Review
  10. 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

4 authors at 1 institution in 1 country.

Erika B DugoNational Institutes of Health RCMI-Center for Environmental Health, Jackson State University, USA.
Clement G YedjouNational Institutes of Health RCMI-Center for Environmental Health, Jackson State University, USA.
Jacqueline J StevensNational Institutes of Health RCMI-Center for Environmental Health, Jackson State University, USA.
Paul B TchounwouNational Institutes of Health RCMI-Center for Environmental Health, Jackson State University, USA.
Jackson State University · US

Funding

RCMI-Center for Environmental HealthG12MD007581 · NIMHD · JACKSON STATE UNIVERSITY · PI TCHOUNWOU, PAUL B. · 2012 to 2017
$11.2M
NIMHD NIH HHS G12 MD007581
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC), the dominant form of primary liver cancer, is the sixth most common cancer in the world with more than 700,000 people diagnosed annually. Arsenic trioxide (ATO) has been shown to be a potent anticancer agent in various carcinomas, proving particularly effective in the clinical treatment of relapsed and refractory acute promyelocytic leukemia. However, its bioactivity and molecular mechanisms against HCC has not been fully studied. Using human HCC (HepG2) cells as a test model, we studied the effects of ATO and examined the role of oxidative stress (OS) and apoptosis in cytotoxicity. OS biomarkers showed a significant increase (p< 0.05) of malondialdehyde concentrations, and a gradual decrease of antioxidant enzymes (GPx & CAT) activities with increasing ATO doses. Flow cytometry data showed a dose dependent increase in annex in V positive cells and caspase 3 activities. These results were confirmed by data of the DNA laddering assay showing a clear evidence of nucleosomal DNA fragmentation, as well as data from Western blotting showing a significant modulation of specific apoptotic related proteins, including the activation of p53 and p21 expression and the down-regulation of Bcl-2 expression in ATO-treated cells. Taken together, our research demonstrates that ATO has a potential therapeutic effect against HCC, and its cytotoxicity may be mediated via oxidative stress and activation of the mitochondrial or intrinsic pathway of apoptosis.

Indexed as

ApoptosisATODNA fragmentationHepG2 cellsOxidative stress

Identifiers

PMID29214213
PMCPMC5713642
OpenAlexW3004085817

What OpenQuestion holds

Textmetadata
LicenceTDM
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.