Evidence map›Paper›PMID 40389113›Full record

ArticleJournal of advanced research2026

Heme oxygenase 1 (HO-1) is a drug target for reversing cisplatin resistance in non-small cell lung cancer.

Jie Mei, Hui-Xiang Tian, Xiao-Ye Zhang, Yuan-Shen Chen, Lei-Yun Wang, Zhao Zhang, Yu-Long Zhang, Ding-Chao Rong, Jun Zeng, Min Dong and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. PCK2 Inhibition Reverses Cisplatin Resistance of Non-Small Cell Lung Cancer by Triggering Ferroptosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

15 authors.

Jie MeiDepartment of Clinical Pharmacology, Xiangya Hospital, Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics and National Clinical Research Center for Geriatric Disorders, Engineering Research Center of Applied Technology of Pharmacogenomics (Ministry of Education, China), Key Laboratory of Pharmacomicrobiomics of Hunan Province, Central South University, Changsha 410078, People's Republic of China; Central Laboratory of Hunan Cancer Hospital, Central South University, Changsha 410013, People's Republic of China; FuRong Laboratory, Changsha 410078 Hunan, People's Republic of China; Oujiang Laboratory, Key Laboratory of Alzheimer's Disease of Zhejiang Province, Institute of Aging, Wenzhou Medical University, Wenzhou 325000, People's Republic of China.
Hui-Xiang TianDepartment of Clinical Pharmacology, Xiangya Hospital, Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics and National Clinical Research Center for Geriatric Disorders, Engineering Research Center of Applied Technology of Pharmacogenomics (Ministry of Education, China), Key Laboratory of Pharmacomicrobiomics of Hunan Province, Central South University, Changsha 410078, People's Republic of China.
Xiao-Ye ZhangDepartment of Clinical Pharmacology, Xiangya Hospital, Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics and National Clinical Research Center for Geriatric Disorders, Engineering Research Center of Applied Technology of Pharmacogenomics (Ministry of Education, China), Key Laboratory of Pharmacomicrobiomics of Hunan Province, Central South University, Changsha 410078, People's Republic of China; Central Laboratory of Hunan Cancer Hospital, Central South University, Changsha 410013, People's Republic of China.
Yuan-Shen ChenThe First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou 510080, People's Republic of China.
Lei-Yun WangDepartment of Pharmacy, Traditional Chinese and Western Medicine Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, People's Republic of China.
Zhao ZhangCentral South University Xiangya Medical School, Changsha 410013, People's Republic of China.
Yu-Long ZhangDepartment of Clinical Pharmacology, Xiangya Hospital, Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics and National Clinical Research Center for Geriatric Disorders, Engineering Research Center of Applied Technology of Pharmacogenomics (Ministry of Education, China), Key Laboratory of Pharmacomicrobiomics of Hunan Province, Central South University, Changsha 410078, People's Republic of China.
Ding-Chao RongDepartment of Orthopedics, The First Affiliated Hospital of Shaoyang University, Shaoyang 422000, People's Republic of China.
Jun ZengDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha 410008, People's Republic of China.
Min DongPharmaceutical College, Guangxi Medical University, Nanning 530021, People's Republic of China.
Yang GaoDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha 410008, People's Republic of China.
Ji-Ye YinDepartment of Clinical Pharmacology, Xiangya Hospital, Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics and National Clinical Research Center for Geriatric Disorders, Engineering Research Center of Applied Technology of Pharmacogenomics (Ministry of Education, China), Key Laboratory of Pharmacomicrobiomics of Hunan Province, Central South University, Changsha 410078, People's Republic of China. Electronic address: yinjiye@csu.edu.cn.
Hai-Jun WuDepartment of Oncology, Xiangya Hospital of Central South University, Changsha 410008, People's Republic of China. Electronic address: wuhaijun@csu.edu.cn.
Peng-Yuan WangOujiang Laboratory, Key Laboratory of Alzheimer's Disease of Zhejiang Province, Institute of Aging, Wenzhou Medical University, Wenzhou 325000, People's Republic of China. Electronic address: py.wang@ojlab.ac.cn.
Wei ZhangDepartment of Clinical Pharmacology, Xiangya Hospital, Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics and National Clinical Research Center for Geriatric Disorders, Engineering Research Center of Applied Technology of Pharmacogenomics (Ministry of Education, China), Key Laboratory of Pharmacomicrobiomics of Hunan Province, Central South University, Changsha 410078, People's Republic of China; Central Laboratory of Hunan Cancer Hospital, Central South University, Changsha 410013, People's Republic of China; FuRong Laboratory, Changsha 410078 Hunan, People's Republic of China; The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou 510080, People's Republic of China. Electronic address: csuzhangwei@csu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPlatinum-based drugs, the most widely used chemotherapeutic drugs in clinical oncology, have long faced the problem of drug resistance, which is urgently in need of resolution. Identifying biomarkers of drug resistance may help reduce platinum resistance and improve therapeutic efficacy.

objectivesThis study aims to identify potential biomarkers associated with the development of cisplatin resistance in non-small cell lung cancer (NSCLC) and explore mechanisms to overcome chemoresistance.

methodsNSCLC cisplatin resistance cell lines were constructed, and transcriptome sequencing was performed. Results were validated using Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. Molecular docking, proteomics sequencing, and in vitro and in vivo experiments were conducted to evaluate the role of Heme Oxygenase 1 (HO-1) in cisplatin resistance.

resultsNSCLC cisplatin resistance cell lines, GEO and TCGA data identified HMOX1, downstream of Nrf2, as a key drug resistance gene induced by cisplatin. Activation of the Nrf2/HO-1 pathway was found to induce ferroptosis resistance, a critical mechanism of cisplatin resistance. Candidate compounds SB 202190 and Nordihydroguaiaretic acid (NDGA) effectively reactivated ferroptosis by inhibiting HO-1, thereby increasing cisplatin sensitivity.

conclusionThe Nrf2/HO-1 pathway is a significant contributor to cisplatin resistance in NSCLC. Targeting HO-1 with SB 202190 and NDGA presents a promising strategy to overcome resistance and improve chemotherapy outcomes.

Indexed as

Carcinoma, Non-Small-Cell LungCisplatinDrug Resistance, NeoplasmHeme Oxygenase-1Lung NeoplasmsAnimalsAntineoplastic AgentsCell Line, TumorFerroptosisGene Expression Regulation, NeoplasticHumansMiceMice, NudeMolecular Docking SimulationNF-E2-Related Factor 2Xenograft Model Antitumor AssaysAntineoplastic AgentsCisplatinHeme Oxygenase-1HMOX1 protein, humanNFE2L2 protein, humanNF-E2-Related Factor 2Drug resistanceFerroptosisHO-1Nrf2 pathwayNSCLC

Identifiers

PMID40389113
PMCPMC12869221

What Socratic holds

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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 Socratic graph.