Evidence map›Paper›PMID 40897821›Full record

ArticleBritish journal of cancer2025

m1A methylase TRMT6 promotes neuroblastoma development by demethylating SST mRNA in an m1A/YTHDF2-dependent manner.

Xinxin Zhang, Huiran Lin, Huimin Yin, Yufeng Han, Liping Chen, Mengzhen Zhang, Hongxia Chen, Jing He, Zhenjian Zhuo

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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. RNA modifications in cancer and their detection: a review.Japanese journal of clinical oncology · 2026
    Review
  4. 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

9 authors.

Xinxin Zhang *Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China.
Huiran Lin *Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China.
Huimin YinDepartment of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China.
Yufeng HanDepartment of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China.
Liping ChenDepartment of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China.
Mengzhen ZhangDepartment of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China.
Hongxia ChenState Key Laboratory of Chemical Oncogenomics, Shenzhen Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, Guangdong, China.
Jing HeDepartment of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China. hejing198374@gmail.com.ORCID http://orcid.org/0000-0002-1954-2892
Zhenjian ZhuoDepartment of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China. zhenjianzhuo@163.com.ORCID http://orcid.org/0000-0003-0142-4086

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32300473National Natural Science Foundation of China (National Science Foundation of China) 82173593
6 · The paper itself

Abstract

backgroundm1A, a prevalent RNA modification found in various RNA species, has recently been reported to modulate cancer progression. However, its effects on neuroblastoma remain uninvestigated.

methodsThe PCAT database was utilized to analyze the mRNA levels and survival probabilities of m1A regulator genes (TRMT6, TRMT61A, ALKBH1, and ALKBH3) in neuroblastoma patients. Silencing and recovery of TRMT6 were employed to investigate its role in neuroblastoma in vitro and in vivo. m1A-seq and RIP-qPCR were performed to identify and confirm the downstream targets of TRMT6. Additionally, Actinomycin D treatment was administered to assess mRNA stability.

resultsm1A transmethylase TRMT6 expression was significantly elevated in high-risk and late-stage neuroblastoma patients. Functionally, TRMT6 promotes the malignancy of neuroblastoma cells in vitro and promotes tumor growth and metastasis in vivo. Mechanistically, TRMT6 reduces SST mRNA levels by inhibiting its stability in an m1A-YTHDF2-dependent manner, thereby promoting the development of neuroblastoma. Furthermore, SST analog octreotide suppresses neuroblastoma cell malignancy, tumor growth, and metastasis.

conclusionsTRMT6 mediates m1A modification of SST to promote neuroblastoma progression, suggesting that targeting TRMT6 may be a novel potential therapeutic approach for treating neuroblastoma.

Indexed as

MethyltransferasesNeuroblastomaRNA-Binding ProteinsRNA, MessengerAnimalsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudeXenograft Model Antitumor AssaysMethyltransferasesRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID40897821
PMCPMC12572163

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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.