Evidence map›Paper›PMID 24921657›Full record

ArticlePloS one2014

An increase in reactive oxygen species by deregulation of ARNT enhances chemotherapeutic drug-induced cancer cell death.

Jiunn-Min Shieh, Chih-Jie Shen, Wei-Chiao Chang, Hung-Chi Cheng, Ya-Yi Chan, Wan-Chen Huang, Wen-Chang Chang, Ben-Kuen Chen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 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
1.1field-weighted citation impact, top 24% 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, 25 citations in OpenAlex.

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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

8 authors at 4 institutions in 1 country.

Jiunn-Min ShiehDepartment of Internal Medicine, Chi Mei Medical Center, Tainan, Taiwan, ROC; The Center of General Education, Chia Nan University of Pharmacy and Science, Tainan, Taiwan, ROC.
Chih-Jie ShenInstitute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan, ROC.
Wei-Chiao ChangDepartment of Clinical Pharmacology, and Master Program for Clinical Pharmacogenomics and Pharmacoproteomics, School of Pharmacology, Taipei Medical University, Taipei, Taiwan; Department of Pharmacy, Taipei Medical University-Wanfang Hospital, Taipei, Taiwan, ROC.
Hung-Chi ChengInstitute of Biochemistry, National Cheng Kung University, Tainan, Taiwan, ROC.
Ya-Yi ChanDepartment of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Wan-Chen HuangInstitute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan, ROC.
Wen-Chang ChangGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan, ROC.
Ben-Kuen ChenInstitute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan, ROC; Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC; Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan, ROC.
National Cheng Kung University · TWTaipei Medical University · TWChi Mei Medical Center · TWTaipei Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUnique characteristics of tumor microenvironments can be used as targets of cancer therapy. The aryl hydrocarbon receptor nuclear translocator (ARNT) is an important mediator of tumor progression. However, the functional role of ARNT in chemotherapeutic drug-treated cancer remains unclear. METHODOLOGY/PRINCIPAL

findingsHere, we found that knockdown of ARNT in cancer cells reduced the proliferation rate and the transformation ability of those cells. Moreover, cisplatin-induced cell apoptosis was enhanced in ARNT-deficient cells. Expression of ARNT also decreased in the presence of cisplatin through proteasomal degradation pathway. However, ARNT level was maintained in cisplatin-treated drug-resistant cells, which prevented cell from apoptosis. Interestingly, reactive oxygen species (ROS) dramatically increased when ARNT was knocked down in cancer cells, enhancing cisplatin-induced apoptosis. ROS promoted cell death was inhibited in cells treated with the ROS scavenger, N-acetyl-cysteine (NAC). CONCLUSIONS/SIGNIFICANCE: These results suggested that the anticancer activity of cisplatin is attributable to its induction of the production of ROS by ARNT degradation. Targeting ARNT could be a potential strategy to eliminate drug resistance in cancer cells.

Indexed as

Antineoplastic AgentsAryl Hydrocarbon Receptor Nuclear TranslocatorCaspase 3Cell DeathCell Line, TumorCell ProliferationCell Transformation, NeoplasticCisplatinDrug Resistance, NeoplasmEnzyme ActivationGene Knockdown TechniquesHumansNeoplasm InvasivenessNeoplasmsProteolysisReactive Oxygen SpeciesAntineoplastic AgentsAryl Hydrocarbon Receptor Nuclear TranslocatorCaspase 3CisplatinReactive Oxygen SpeciesRNA, Small Interfering

Identifiers

PMID24921657
PMCPMC4055634
OpenAlexW2055685338

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.