Evidence map›Paper›PMID 41644856›Full record

ArticleCell biology and toxicology2026

NAA20-mediated ACF1 lactylation drives neuroblastoma progression through enhancing GCLM-dependent glutathione synthesis.

Bingqiang Han, Min Xu, Qi Wang, Jianwei Lin, Jun Chu, Yunlan Xu, Dapeng Jiang

Abstract read
In one paragraph

Article in Cell biology and toxicology, 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

The trial behind it

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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

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

7 authors.

Bingqiang HanDepartment of Pediatric Orthopedics, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Min XuDepartment of Department of Oncology (Ward 2), Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Qi WangShanghai Key Laboratory for Nucleic Acid Chemistry and Nanomedicine, Institute of Molecular Medicine, State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Jianwei LinDepartment of Department of Oncology (Ward 2), Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Jun ChuDepartment of Pediatric Surgery, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. chujun516@sina.com.
Yunlan XuDepartment of Pediatric Orthopedics, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. xylproscmc@163.com.
Dapeng JiangDepartment of Department of Oncology (Ward 2), Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. jdp509@163.com.

Funding

Shanghai Hospital Development Center Foundation SHDC22022306
6 · The paper itself

Abstract

Neuroblastoma (NBL) is a pediatric malignancy with poor prognosis in high-risk cases. This study explores the function of albumin conformation factor 1 (ACF1) in NBL progression and delves into the underpinning mechanism. Exome and transcriptome sequencing were applied to analyze ACF1 mutations/expression in NBL tissues versus controls. ACF1 was knocked down in NBL cell lines (KELLY, BE2C, N2a) for in vitro assays (viability, proliferation, migration, apoptosis, therapy sensitivity) or in vivo xenograft/metastasis models with radiation/cisplatin. Mechanisms were probed via RNA-sequencing, chromatin immunoprecipitation, luciferase assays, co-immunoprecipitation, and immunofluorescence assays. Expression patterns and the correlations between ACF1, GCLM, and NAA20 were detected in human NBL tissue microarrays. ACF1 mutations and elevated expression correlated with advanced tumor staging, high-risk factors, and unfavorable prognosis in NBL datasets and TMAs. ACF1 knockdown suppressed NBL cell proliferation, mobility, and in vivo tumor growth/metastasis, while enhancing cisplatin/radiation sensitivity and apoptosis. Mechanistically, ACF1 knockdown reduced GCLM transcription via decreased H3K27ac/H3K4me3/Myc at its promoter, elevating lipid peroxidation and lowering glutathione (GSH) levels. Lactate induced ACF1 lactylation and nuclear translocation, promoted by NAA20 interaction (enhanced by lactate). NAA20 knockdown phenocopied ACF1 effects, rescued by GCLM overexpression. NAA20 and GCLM were upregulated in NBL datasets/TMAs. This study suggests that the NAA20-mediated ACF1 lactylation drives GCLM-dependent GSH synthesis, promoting NBL cell growth and metastasis. Targeting this axis may improve therapy response.

Indexed as

GlutathioneNeuroblastomaN-Terminal Acetyltransferase AAnimalsApoptosisCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeGlutathioneN-Terminal Acetyltransferase AACF1GCLMGlutathioneLactylationNAA20

Identifiers

PMID41644856
PMCPMC12906602

What Socratic holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.