Evidence map›Paper›PMID 26029997›Full record

ArticleOncotarget2015

Redox effects and cytotoxic profiles of MJ25 and auranofin towards malignant melanoma cells.

Marijke C C Sachweh, William C Stafford, Catherine J Drummond, Anna R McCarthy, Maureen Higgins, Johanna Campbell, Bertha Brodin, Elias S J Arnér, Sonia Laín

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Synthesis and in vitro characterization of [EJNMMI radiopharmacy and chemistry · 2025
    Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Redox-Related Proteins in Melanoma Progression.Antioxidants (Basel, Switzerland) · 2022
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
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  18. Article
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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

9 authors at 2 institutions in 2 countries.

Marijke C C SachwehDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
William C StaffordDivision of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Catherine J DrummondDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Anna R McCarthyDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Maureen HigginsCentre for Oncology and Molecular Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, Tayside, United Kingdom.
Johanna CampbellCentre for Oncology and Molecular Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, Tayside, United Kingdom.
Bertha BrodinDepartment of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
Elias S J ArnérDivision of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Sonia LaínDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Karolinska Institutet · SEUniversity of Dundee · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant melanoma is the most dangerous type of skin cancer. Although recent progress in treatment has been achieved, lack of response, drug resistance and relapse remain major problems. The tumor suppressor p53 is rarely mutated in melanoma, yet it is inactive in the majority of cases due to dysregulation of upstream pathways. Thus, we screened for compounds that can activate p53 in melanoma cells. Here we describe effects of the small molecule MJ25 (2-{[2-(1,3-benzothiazol-2-ylsulfonyl)ethyl]thio}-1,3-benzoxazole), which increased the level of p53-dependent transactivation both as a single agent and in combination with nutlin-3. Furthermore, MJ25 showed potent cytotoxicity towards melanoma cell lines, whilst having weaker effects against human normal cells. MJ25 was also identified in an independent screen as an inhibitor of thioredoxin reductase 1 (TrxR1), an important selenoenzyme in the control of oxidative stress and redox regulation. The well-characterized TrxR inhibitor auranofin, which is FDA-approved and currently in clinical trials against leukemia and a number of solid cancers, displayed effects comparable with MJ25 on cells and led to eradication of cultured melanoma cells at low micromolar concentrations. In conclusion, auranofin, MJ25 or other inhibitors of TrxR1 should be evaluated as candidate compounds or leads for targeted therapy of malignant melanoma.

Indexed as

AnimalsAntineoplastic AgentsAuranofinBenzothiazolesBenzoxazolesCell Line, TumorCell SurvivalEnzyme ActivationGlutathioneGlutathione ReductaseHCT116 CellsHumansImidazolesIndolesMelanomaMiceAntineoplastic AgentsAuranofinBenzothiazolesBenzoxazolesGlutathioneGlutathione ReductaseImidazolesIndolesMJ25 compoundnutlin 3PiperazinesReactive Oxygen SpeciesSulfonamidesSulfonesThioredoxin Reductase 1TP53 protein, humanTumor Suppressor Protein p53TXNRD1 protein, humanVemurafenibauranofinmalignant melanomap53thioredoxin reductase 1vemurafenib

Identifiers

PMID26029997
PMCPMC4599284
OpenAlexW2133187883

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.