Evidence map›Paper›PMID 42829402›Full record

ArticleApoptosis : an international journal on programmed cell death2026

Ru3: a novel ruthenium-based compound overcomes cisplatin resistance in non-small cell lung cancer via the E2F2-IGFBP3-GPX4 pathway.

Yiting Lu, Shiming Wu, Ying Jiang, Meishu Wang, Xinyu Liao, Jian Zhang, Junqi Xiang, Hua Yang, Min Yu, Jiang Min and 2 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Yiting Lu *Department of General Surgery, Chongqing Academy of Medical Sciences, Chongqing General Hospital, School of Medicine, Chongqing University, Chongqing, 401120, China.ORCID http://orcid.org/0009-0007-6042-5448
Shiming Wu *Chongqing Health Center for Women and Children, Chongqing, 400700, PR China.
Ying JiangDepartment of Biochemistry and Molecular Biology, and Molecular Medicine and Cancer Research Center, College of Basic Medical Sciences, Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Meishu WangCollege of Pharmaceutical Sciences, Southwest University, Chongqing, 400715, PR China.
Xinyu LiaoDepartment of Biochemistry and Molecular Biology, and Molecular Medicine and Cancer Research Center, College of Basic Medical Sciences, Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Jian ZhangDepartment of Biochemistry and Molecular Biology, and Molecular Medicine and Cancer Research Center, College of Basic Medical Sciences, Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Junqi XiangDepartment of Biochemistry and Molecular Biology, and Molecular Medicine and Cancer Research Center, College of Basic Medical Sciences, Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Hua YangDepartment of General Surgery, Chongqing Academy of Medical Sciences, Chongqing General Hospital, School of Medicine, Chongqing University, Chongqing, 401120, China.
Min YuDepartment of General Surgery, Chongqing Academy of Medical Sciences, Chongqing General Hospital, School of Medicine, Chongqing University, Chongqing, 401120, China.
Jiang MinGastrointestinal Surgery Department, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. hustminjiang@126.com.
Chen FuCollege of Pharmaceutical Sciences, Southwest University, Chongqing, 400715, PR China. fuchen0794@swu.edu.cn.
Yunlong LeiDepartment of Biochemistry and Molecular Biology, and Molecular Medicine and Cancer Research Center, College of Basic Medical Sciences, Chongqing Medical University, Chongqing, 400016, People's Republic of China. leiyunlong@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin resistance remains a major hurdle in non-small cell lung cancer (NSCLC) treatment. Here, we designed and synthesized a novel ruthenium-based compound, which selectively kills cisplatin-resistant NSCLC cells while sparing parental cells. Mechanistically, Ru3 triggers mitochondrial damage and reactive oxygen species (ROS) accumulation. In addition, it upregulates the transcription factor E2F2, which directly represses IGFBP3 expression. IGFBP3 normally scavenges ROS via the GPX4 system; thus, E2F2-mediated IGFBP3 suppression disrupts this antioxidant defense, exacerbating ROS levels and cell death. Notably, cisplatin-resistant cells exhibit elevated GPX4 and IGFBP3 expression, making them particularly vulnerable to Ru3. This study elucidates the E2F2-IGFBP3-GPX4 axis as a novel therapeutic vulnerability and highlights Ru3 as a promising agent for refractory NSCLC.

Indexed as

Antineoplastic AgentsCarcinoma, Non-Small-Cell LungCisplatinDrug Resistance, NeoplasmInsulin-Like Growth Factor Binding Protein 3Lung NeoplasmsRutheniumRuthenium CompoundsAnimalsApoptosisCarbolinesCell Line, TumorGlutathione PeroxidaseHumansReactive Oxygen SpeciesSignal TransductionAntineoplastic AgentsCarbolinesCisplatinGlutathione PeroxidaseInsulin-Like Growth Factor Binding Protein 3Reactive Oxygen SpeciesRSL3 compoundRutheniumRuthenium CompoundsCisplatin resistance lung cancerE2F2IGFBP3ROSRuthenium

Identifiers

PMID42829402
PMCPMC13633971

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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.