Evidence map›Paper›PMID 40313939›Full record

ArticleFrontiers in immunology2025

ALDOC promotes neuroblastoma progression and modulates sensitivity to chemotherapy drugs by enhancing aerobic glycolysis.

Yunpeng Chen, Haixia Zhu, Yishu Luo, Tianyue Xie, Youyang Hu, Zhiwei Yan, Weichao Ji, YaXuan Wang, Qiyou Yin, Hua Xian

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Review
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  6. H4K5 lactylation - ENO2 loop drives glycolysis and HCC progression.JHEP reports : innovation in hepatology · 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

10 authors.

Yunpeng Chen *School of Medicine, Nantong University, Nantong, China.
Haixia Zhu *Cancer Research Center Nantong, Nantong Tumor Hospital, Nantong, Jiangsu, China.
Yishu Luo *School of Medicine, Nantong University, Nantong, China.
Tianyue Xie *Department of Endocrinology, Affiliated Hospital of Nantong University, Nantong, China.
Youyang HuDepartment of Cardiothoracic Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Zhiwei YanSchool of Medicine, Nantong University, Nantong, China.
Weichao JiSchool of Medicine, Nantong University, Nantong, China.
YaXuan WangDepartment of Urology, Nantong Tumor Hospital, Nantong, China.
Qiyou YinDepartment of Paediatric Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Hua XianDepartment of Paediatric Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Neuroblastoma (NB), a malignant extracranial solid tumor originating from the sympathetic nervous system, exhibits poor prognosis in high-risk cases, with a 5-year overall survival rate below 50%. Glycolysis has been implicated in NB pathogenesis, and targeting glycolysis-related pathways shows therapeutic potential. This study investigates the role of the glycolysis-associated gene ALDOC in NB pathogenesis and its impact on chemotherapy sensitivity. Methods: Transcriptomic data from NB patients were analyzed to identify ALDOC as an independent risk factor for high-risk NB. Protein expression levels of ALDOC were assessed in NB cells versus normal cells using immunoblotting. Functional experiments, including proliferation and migration assays, were conducted in ALDOC-interfered NB cell lines. Glycolytic activity was evaluated by measuring glucose uptake, lactate production, and ATP generation. Additionally, the sensitivity of ALDOC-downregulated NB cells to cisplatin and cyclophosphamide was tested to explore its role in chemotherapy response. Results: ALDOC was identified as a high-risk prognostic marker in NB, with elevated protein expression in NB cells compared to normal controls. Silencing ALDOC significantly inhibited NB cell proliferation and migration. Glycolytic activity was markedly reduced in ALDOC-downregulated cells, evidenced by decreased glucose uptake, lactate production, and ATP levels. Furthermore, ALDOC suppression enhanced NB cell sensitivity to cisplatin and cyclophosphamide, suggesting a glycolysis-dependent mechanism underlying chemotherapy resistance. Discussion: Our findings highlight ALDOC as a critical driver of NB progression through glycolysis acceleration, with implications for therapeutic targeting. The observed increase in chemotherapy sensitivity upon ALDOC inhibition underscores its potential as a biomarker for treatment optimization. However, the complexity of glycolysis regulation, involving multiple genes and pathways, necessitates further mechanistic studies to clarify ALDOC's specific role. Despite this limitation, our work emphasizes the importance of aerobic glycolysis in NB pathogenesis and provides a foundation for developing novel therapeutic strategies targeting ALDOC or associated pathways. Future research should explore interactions between ALDOC and other glycolytic regulators to refine combinatorial treatment approaches.

Indexed as

Antineoplastic AgentsDrug Resistance, NeoplasmGlycolysisNeuroblastomaBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationCisplatinCyclophosphamideDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMalePrognosisAntineoplastic AgentsBiomarkers, TumorCisplatinCyclophosphamideaerobic glycolysisALDOCdrug sensitivityMYCNneuroblastoma

Identifiers

PMID40313939
PMCPMC12043483

What Socratic holds

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LicenceCC BY
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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.