Evidence map›Paper›PMID 42292604›Full record

ArticleTranslational pediatrics2026

Enqing Zhou, Xiaoran Du, Deqian Chen, Shuyang Dai, Yong Zhan, Yi Li, Yifei Lu, Lian Chen, Kuiran Dong, Ran Yang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational pediatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Enqing Zhou *Department of Pediatric Surgery, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Birth Defect, Fudan University, Shanghai, China.
Xiaoran Du *Department of Pediatric Surgery, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Birth Defect, Fudan University, Shanghai, China.
Deqian ChenDepartment of Pediatric Surgery, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Birth Defect, Fudan University, Shanghai, China.
Shuyang DaiDepartment of Pediatric Surgery, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Birth Defect, Fudan University, Shanghai, China.
Yong ZhanDepartment of Pediatric Surgery, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Birth Defect, Fudan University, Shanghai, China.
Yi LiDepartment of Pediatric Surgery, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Birth Defect, Fudan University, Shanghai, China.
Yifei LuDepartment of Pediatric Surgery, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Birth Defect, Fudan University, Shanghai, China.
Lian ChenDepartment of Pathology, Children's Hospital of Fudan University, Fudan University, Shanghai, China.
Kuiran DongDepartment of Pediatric Surgery, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Birth Defect, Fudan University, Shanghai, China.
Ran YangDepartment of Pediatric Surgery, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Birth Defect, Fudan University, Shanghai, China.
Rui DongDepartment of Pediatric Surgery, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Birth Defect, Fudan University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Active oxidative phosphorylation is increasingly recognized as a defining metabolic feature of high-risk neuroblastoma (NB). NADH:ubiquinone oxidoreductase subunit S6 (NDUFS6), encoding an essential subunit of mitochondrial respiratory chain complex I, plays a critical role in sustaining oxidative phosphorylation. Nevertheless, its precise contribution to NB pathogenesis and progression remains largely undefined. Methods: To characterize the expression landscape of NDUFS6, publicly available single-cell and bulk RNA sequencing datasets were analyzed, and the GSE49710 dataset was used to evaluate its prognostic significance. Immunohistochemical staining was performed to assess NDUFS6 expression across distinct clinical subgroups. Stable SK-N-BE(2) and SH-SY5Y cell lines with NDUFS6 overexpression or knockdown were generated to conduct functional assays, including Cell Counting Kit-8 (CCK-8) proliferation, colony formation and Transwell assays. Transcriptomic alterations induced by NDUFS6 modulation were profiled by RNA sequencing. In parallel, a structure-based virtual screening of the MedChemExpress (MCE) Bioactive Compound Library Plus was conducted to identify candidate small-molecule inhibitors of NDUFS6, with selected compounds evaluated for cytotoxicity in NB cells. Results: NDUFS6 expression was significantly upregulated in high-risk NB (HR-NB) and was positively associated with disease progression and poor prognosis. Functional assays revealed that NDUFS6 knockdown suppressed proliferation, invasion, and migration of NB cells, whereas its overexpression promoted these malignant behaviors. Transcriptomic analysis revealed that high NDUFS6 expression activated pathways related to energy metabolism and adenosine triphosphate (ATP) synthesis, while concurrently suppressing neuronal differentiation and immune activation. Structure-based virtual screening identified several candidate inhibitors of NDUFS6, including guanosine 5'-triphosphate (disodium salt), 1,4-β-D-xylopentaose, and deferoxamine. Subsequent drug sensitivity assays demonstrated that guanosine-5'-triphosphate (disodium salt) exerted potent inhibitory effects in both MYCN-amplified and non-amplified NB cell lines. These findings underscore the oncogenic role of NDUFS6 and highlight its potential as a therapeutic target for precision treatment in HR-NB. Conclusions: NDUFS6 is significantly upregulated in HR-NB and contributes to tumor aggressiveness by promoting proliferation, migration, and invasion, accompanied by activation of metabolic pathways and suppression of neuronal differentiation and immune responses. Virtual screening identified guanosine 5'-triphosphate (disodium salt) as a potential NDUFS6 inhibitor with efficacy in both MYCN-amplified and non-amplified cells, highlighting NDUFS6 as a promising therapeutic target and providing a rationale for targeted intervention in HR-NB.

Indexed as

guanosine 5’-triphosphate (disodium salt)NADH:ubiquinone oxidoreductase subunit S6 (NDUFS6)Neuroblastoma (NB)oxidative phosphorylationtargeted therapy

Identifiers

PMID42292604
PMCPMC13263444

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.