Evidence map›Paper›PMID 40983627›Full record

ArticleBritish journal of cancer2025

ENO1 promotes cancer metastasis via stimulating metabolism reprogramming in osteosarcoma.

Peng Huang, Shiwei He, Zhi Qi, Yaxier Nijiati, Junfeng Wang, Zichen Lin, Yangyang Ma, Rui Dong, Gong Chen, Bo Ning

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 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. Review
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

10 authors.

Peng Huang *Children's Hospital of Fudan University, National Children's Medical Center Department of Orthopaedics Surgery, Shanghai, China.
Shiwei He *Children's Hospital of Fudan University, National Children's Medical Center Department of Pediatric Surgery, Shanghai, China.
Zhi Qi *Children's Hospital of Fudan University, National Children's Medical Center Department of Orthopaedics Surgery, Shanghai, China.
Yaxier NijiatiChildren's Hospital of Fudan University, National Children's Medical Center Department of Orthopaedics Surgery, Shanghai, China.
Junfeng WangChildren's Hospital of Fudan University, National Children's Medical Center Department of Orthopaedics Surgery, Shanghai, China.
Zichen LinChildren's Hospital of Fudan University, National Children's Medical Center Department of Orthopaedics Surgery, Shanghai, China.
Yangyang MaChildren's Hospital of Fudan University, National Children's Medical Center, Department of Pathology, Shanghai, China.
Rui DongChildren's Hospital of Fudan University, National Children's Medical Center Department of Pediatric Surgery, Shanghai, China. rdong@fudan.edu.cn.ORCID http://orcid.org/0000-0001-9645-4768
Gong ChenChildren's Hospital of Fudan University, National Children's Medical Center Department of Pediatric Surgery, Shanghai, China. chengongzlp@hotmail.com.ORCID http://orcid.org/0000-0003-3351-0819
Bo NingChildren's Hospital of Fudan University, National Children's Medical Center Department of Orthopaedics Surgery, Shanghai, China. ningbo@fudan.edu.cn.ORCID http://orcid.org/0000-0002-9752-2459

Funding

National Natural Science Foundation of China (National Science Foundation of China) No. 82272441Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) No. 22Y11912200
6 · The paper itself

Abstract

backgroundThis study aims to unravel the underlying mechanisms of osteosarcoma (OS) metastasis by single-cell RNA-sequencing.

methodsTen pediatrics OS samples were analyzed using scRNA-seq and divided into three groups: primary tumor without lung metastasis (Pri_non_MT), primary tumor with lung metastasis (Pri_MT), and lung metastasis site (MT). Candidate genes associated with metastasis were identified by bioinformatics analysis and was confirmed at mRNA and protein levels in OS tissues. The function of candidate gene was identified in vitro and in vivo. Bulk RNA sequencing was used to explore downstream mechanism after candidate gene silenced.

resultsA total of 17 cell clusters were identified. ENO1 was selected as the candidate gene and was significantly expressed in Pri_MT and MT groups. In OS tissues, ENO1 significantly overexpressed in patients with lung metastasis compared to those without. Knocking down ENO1 resulted in a marked decrease in migration and invasion in vitro and a reduction in lung metastasis in vivo. Additionally, ENO1 suppression resulted in shifting the primary ATP production pathway from glycolysis to oxidative phosphorylation.

conclusionsOur findings highlight ENO1 as a key regulator of glycolysis and metastasis in osteosarcoma, offering a novel therapeutic target for OS treatment.

Indexed as

Bone NeoplasmsDNA-Binding ProteinsLung NeoplasmsOsteosarcomaPhosphopyruvate HydrataseTumor Suppressor ProteinsAnimalsBiomarkers, TumorCell Line, TumorCell MovementChildFemaleGene Expression Regulation, NeoplasticGlycolysisHumansMaleBiomarkers, TumorDNA-Binding ProteinsENO1 protein, humanPhosphopyruvate HydrataseTumor Suppressor Proteins

Identifiers

PMID40983627
PMCPMC12644477

What OpenQuestion holds

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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.