Evidence map›Paper›PMID 42048629›Full record

ArticleBlood advances2026

ENO1 promotes acute myeloid leukemia progression through SCD1-mediated lipid metabolism reprogramming.

Yijun Wu, Li Gao, Fang Fang, Zhiheng Li, Yixin Hu, Yongping Zhang, Chenwei Yang, Zhongling Wei, Xin Liu, Ying Yang and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Blood advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Yijun WuDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.ORCID 0009-0006-2112-5189
Li GaoDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.ORCID 0000-0001-5743-8474
Fang FangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Zhiheng LiInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Yixin HuDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.
Yongping ZhangDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.ORCID 0000-0003-2647-6739
Chenwei YangDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.ORCID 0009-0008-5326-7274
Zhongling WeiDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.
Xin LiuDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.ORCID 0009-0007-7138-2463
Ying YangDepartment of Pediatrics, Affiliated Hospital of Guizhou Medical University, Guiyang, China.
Fenli ZhangDepartment of Pediatrics, Affiliated Hospital of Guizhou Medical University, Guiyang, China.ORCID 0009-0009-2172-8571
Weiliang ZhangDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.
Kaixuan SunDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.
Yizhen LiDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.
Chun YangInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.ORCID 0000-0002-0505-6092
Jian PanInstitute of Pediatric Research, Children's Hospital of Soochow University, Suzhou, China.
Shaoyan HuDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, China.ORCID 0000-0002-3386-6957

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

abstractα-Enolase (ENO1) is a potential therapeutic target in acute myeloid leukemia (AML), owing to its elevated expression in AML cells. In this study, we investigated the association between high ENO1 expression, accelerated tumor progression, and poor AML prognosis. Transcriptomic and metabolomic analyses indicated that ENO1 directly modulates lipid metabolism via regulating stearoyl-coenzyme A desaturase 1 (SCD1) expression. We further demonstrated that ENO1 functions as a DNA-binding protein, interacting with the SCD1 promoter region to enhance SCD1 transcription. This results in increased synthesis of monounsaturated fatty acids, leading to increased resistance to lipid peroxidation and ferroptosis. Based on these results, we found that SSI-4, an SCD1 inhibitor, could enhance chemosensitivity of daunorubicin (DNR), which can induce ferroptosis in tumor cells, effectively reducing the resistance to ferroptosis in AML cells exhibiting high ENO1 expression. Overall, our study elucidates the mechanism of ENO1 that promotes SCD1 transcription, driving lipid reprogramming and ferroptosis resistance within AML. In addition, it highlights the therapeutic potential of combining SCD1 inhibition with DNR for patients with AML with elevated ENO1 expression levels.

Indexed as

DNA-Binding ProteinsLeukemia, Myeloid, AcuteLipid MetabolismPhosphopyruvate HydrataseStearoyl-CoA DesaturaseTumor Suppressor ProteinsCell Line, TumorDaunorubicinDisease ProgressionFerroptosisGene Expression Regulation, LeukemicHumansMetabolic ReprogrammingDaunorubicinDNA-Binding ProteinsENO1 protein, humanPhosphopyruvate HydrataseSCD protein, humanStearoyl-CoA DesaturaseTumor Suppressor Proteins

Identifiers

PMID42048629
PMCPMC13383233

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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.