Evidence map›Paper›PMID 40495487›Full record

ArticleBMB reports2025

Auranofin, an antirheumatic drug, shows anticancer stem cell potential via suppression of the Stat3 signal.

Seung-Yeon Ko, Yuna Kim, Jin Sun Chung, Young Bin Kim, Su-Lim Kim, Dong-Sun Lee, Kyung-Hee Chun, Hack Sun Choi

Abstract read
In one paragraph

Article in BMB reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Nuclear Galectin-1 Drives Cancer Progression throughInternational journal of biological sciences · 2026
    Article
  3. 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

8 authors.

Seung-Yeon KoDepartment of Biochemistry & Molecular Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul 03722, Korea.
Yuna KimDepartment of Biochemistry & Molecular Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul 03722, Korea.
Jin Sun ChungDepartment of Biochemistry & Molecular Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul 03722, Korea.
Young Bin KimDepartment of Biochemistry & Molecular Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul 03722, Korea.
Su-Lim KimFaculty of Biotechnology, College of Applied Life Sciences, Jeju National University, SARI, Jeju 63243, Korea.
Dong-Sun LeeFaculty of Biotechnology, College of Applied Life Sciences, Jeju National University, SARI, Jeju 63243, Korea.
Kyung-Hee ChunDepartment of Biochemistry & Molecular Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul 03722, Korea.
Hack Sun ChoiDepartment of Biochemistry & Molecular Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul 03722, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating data have shown that targeting breast cancer stem cells (CSCs) is an auspicious way for anticancer therapies. This study demonstrated that the antirheumatic drug auranofin is a potent CSC inhibitor with anti-CSC action on breast cancer. This research focused on investigating the effect of auranofin on breast cancer and CSCs and its cellular mechanism. Mammosphere formation, colony formation, levels of CD44high/CD24low, and aldehyde dehydrogenase 1 expression in the cells were evaluated after auranofin treatment. The anti-CSC properties of auranofin were further examined by gel shift assay and cytokine detection. Auranofin suppressed cell growth, colony formation, migration, and mammosphere formation and triggered apoptosis in breast cancer. Auranofin decreased the CD44high/CD24low- and aldehyde dehydrogenaseexpressed subpopulations, as well as the Stat3-DNA interaction and phosphorylated Stat3 level. Auranofin also decreased the extracellular levels of interleukin-8 (IL-8) in the mammosphere media. Auranofin suppressed the Stat3/IL-8 signal and killed CSCs; therefore, it may be a potential target for CSCs. [BMB Reports 2025; 58(7): 293-299].

Indexed as

Antirheumatic AgentsAuranofinNeoplastic Stem CellsSTAT3 Transcription FactorAntineoplastic AgentsApoptosisBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationFemaleHumansInterleukin-8MCF-7 CellsSignal TransductionAntineoplastic AgentsAntirheumatic AgentsAuranofinInterleukin-8STAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID40495487
PMCPMC12313401

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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.