Evidence map›Paper›PMID 41292488›Full record

ArticleRedox report : communications in free radical research2025

The novel thioredoxin reductase inhibitor butaselen suppresses lung cancer by inducing oxidative stress.

Yifan Chen, Guangliang Qiang, Liang Jin, Yan Sun, Guozhou Zhang, Fengling Hu, Jinhui Feng, Feng Wei, Shengxin Zeng, Lixiang Xue and 2 more

Abstract read
In one paragraph

Article in Redox report : communications in free radical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

12 authors.

Yifan ChenInstitute of Medical Innovation and Research, Peking University Third Hospital, Beijing, People's Republic of China.ORCID 0000-0002-2229-9037
Guangliang QiangDepartment of Thoracic Surgery, Peking University Third Hospital, Beijing, People's Republic of China.
Liang JinDepartment of Thoracic Surgery, Peking University Third Hospital, Beijing, People's Republic of China.
Yan SunInstitute of Medical Innovation and Research, Peking University Third Hospital, Beijing, People's Republic of China.
Guozhou ZhangState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, People's Republic of China.
Fengling HuKey Laboratory of Carcinogenesis and Translational Research, Department of Thoracic Surgery I, Peking University Cancer Hospital & Institute, Beijing, People's Republic of China.
Jinhui FengKey Laboratory of Carcinogenesis and Translational Research, Department of Thoracic Surgery I, Peking University Cancer Hospital & Institute, Beijing, People's Republic of China.
Feng WeiDepartment of Orthopaedics, Peking University Third Hospital, Beijing, People's Republic of China.
Shengxin ZengDepartment of Orthopaedics, Peking University Third Hospital, Beijing, People's Republic of China.
Lixiang XueInstitute of Medical Innovation and Research, Peking University Third Hospital, Beijing, People's Republic of China.
Huihui ZengState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, People's Republic of China.
Shaohua MaDepartment of Thoracic Surgery, Peking University Third Hospital, Beijing, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung cancer is one of the leading causes of cancer-related deaths worldwide with limited treatment options available. The anti-tumor effects of the TrxR inhibitor Butaselen (BS/BS1801) on lung cancer and its underlying mechanisms remain unknown.

methodsThis study utilized lung cancer cell lines, LLC1-bearing mice models, and organoids to detect the inhibitory effects of BS on lung cancer. The ROS-induction and apoptotic role of BS on lung cancer cells and molecular mechanisms were assessed with flow cytometry, western blot, Co-IP, real-time PCR, ChIP, reporter gene assay, ELISA, and bisulfite pyrosequencing.

resultsBS can effectively inhibit lung cancer both in vitro and in vivo, by triggering ROS-induced apoptosis. The inactivation of NF-κB and MAPK signaling pathways, along with the activation of PI3K-Akt and HBP1 signaling pathways, are involved in BS's suppression of lung cancer. HBP1 is a novel downstream target of the Trx system. The activation of HBP1 by BS is dependent on ROS accumulation and further leads to the transcriptional inhibition of DNMT1 and the demethylation of the whole genome, as well as the promoters of p21 and HOXA9.

conclusionThe TrxR/Trx inhibitor butaselen suppresses lung cancer by triggering ROS-induced apoptosis. This study provides a novel and effective regimen for treating lung cancer.

Indexed as

Antineoplastic AgentsLung NeoplasmsOrganoselenium CompoundsOxidative StressThioredoxin-Disulfide ReductaseAnimalsApoptosisCell Line, TumorHumansMiceReactive Oxygen SpeciesSignal TransductionAntineoplastic AgentsOrganoselenium CompoundsReactive Oxygen SpeciesThioredoxin-Disulfide ReductaseapoptosisbutaselenDNA methylationhigh-mobility group box-containing protein 1 (HBP1)Lung canceroxidative stressthioredoxin reductaseubiquitination

Identifiers

PMID41292488
PMCPMC12667355

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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.