Evidence map›Paper›PMID 39979690›Full record

ArticleMolecular neurobiology2025

Silencing YTHDF2 Induces Apoptosis of Neuroblastoma Cells In a Cell Line-Dependent Manner via Regulating the Expression of DLK1.

Zhongyan Hua, Baocheng Gong, Zhijie Li

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Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. DLK1: a novel therapeutic target in cancer.Endocrine-related cancer · 2026
    Review
  2. Emerging roles of RNA mInternational journal of oncology · 2026
    Review
  3. Article
  4. Article
  5. 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

3 authors.

Zhongyan Hua *Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China.
Baocheng Gong *Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China.
Zhijie LiDepartment of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China. lizhijie@cmu.edu.cn.ORCID http://orcid.org/0000-0003-2821-0846

Funding

National Natural Science Foundation of China 82002641National Natural Science Foundation of China 82272940the Science and Technology Joint Fund Project of Liaoning Province 2023-MSLH-390the Science and Technology Program of Liaoning Province 2022JH2/20200075the "Xingliao Talents Program" of Liaoning Province XLYC2008010
6 · The paper itself

Abstract

Neuroblastoma (NB) is the most common extracranial malignant solid tumor in children. The complications caused by traditional chemoradiotherapy seriously affect the quality of life of patients with NB. In this study, NGP, KCNR, and SH-SY5Y (SY5Y) cell lines were used. Retinoic acid (RA, 5 µM) was used to treat NB cells for 48 h. siRNAs were used to silence the expression of DLK1 or YTHDF2. Cell confluence was analyzed using IncuCyte ZOOM to evaluate cell proliferation of NB cells. RT-qPCR and western blotting were performed to detect the expression of target molecules. Annexin V/PI staining and Caspase-Glo 3/7 assay were performed to detect cell apoptosis. RNA m6A quantification, MeRIP-qPCR, and RIP-qPCR were performed. Results showed that RA treatment decreased the expression of DLK1 and YTHDF2 in NB cells, and low expression of DLK1 was correlated with good prognosis of patients. Knockdown of the expression of DLK1 or YTHDF2 inhibited cell proliferation and induced apoptosis of SY5Y cells, but not NGP and KCNR cells. Furthermore, we found that there are m6A modification sites in DLK1 mRNA, and the expression of m6A modified DLK1 mRNA increased after RA treatment, and YTHDF2 regulates the expression level of DLK1, and the expression of YTHDF2-bound DLK1 mRNA decreased after RA treatment. These suggest that YTHDF2 may regulate the proliferation and apoptosis of NB cells in a cell line-dependent manner by binding to the m6A modification site of DLK1 mRNA to affect its expression, and YTHDF2 and DLK1 are potential therapeutic targets for patients with NB.

Indexed as

ApoptosisCalcium-Binding ProteinsGene Expression Regulation, NeoplasticGene SilencingIntercellular Signaling Peptides and ProteinsMembrane ProteinsNeuroblastomaRNA-Binding ProteinsCell Line, TumorCell ProliferationHumansRNA, MessengerTretinoinCalcium-Binding ProteinsDLK1 protein, humanIntercellular Signaling Peptides and ProteinsMembrane ProteinsRNA-Binding ProteinsRNA, MessengerTretinoinYTHDF2 protein, humanCell apoptosisDLK1m6ANeuroblastomaYTHDF2

Identifiers

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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.