Evidence map›Paper›PMID 38291517›Full record

ReviewCell communication and signaling : CCS2024

Research progress of N1-methyladenosine RNA modification in cancer.

Yafeng Liu, Shujun Zhang, Xiaohui Gao, Yi Ru, Xinyu Gu, Xinjun Hu

Abstract readVideo-Audio MediaReview
In one paragraph

Review in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
–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

43 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. NNature plants · 2026
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  8. RNA modifications and cancer ferroptosis.Cancer cell international · 2026
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  11. Article
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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

6 authors.

Yafeng Liu *Department of Infectious Diseases, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang, No. 24 Jinghua Road, Jianxi District, 471000, Henan, China.
Shujun Zhang *Department of Infectious Diseases, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang, No. 24 Jinghua Road, Jianxi District, 471000, Henan, China.
Xiaohui GaoDepartment of Oncology, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang, No. 24 Jinghua Road, Jianxi District, 471000, Henan, China.
Yi RuHepatobiliary Pancreatic Surgery, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang, 471000, Henan, China.
Xinyu GuDepartment of Oncology, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang, No. 24 Jinghua Road, Jianxi District, 471000, Henan, China. hkdguxy@163.com.
Xinjun HuDepartment of Infectious Diseases, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang, No. 24 Jinghua Road, Jianxi District, 471000, Henan, China. hxj5129@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

N1-methyladenosine (m1A) is a post-transcriptionally modified RNA molecule that plays a pivotal role in the regulation of various biological functions and activities. Especially in cancer cell invasion, proliferation and cell cycle regulation. Over recent years, there has been a burgeoning interest in investigating the m1A modification of RNA. Most studies have focused on the regulation of m1A in cancer enrichment areas and different regions. This review provides a comprehensive overview of the methodologies employed for the detection of m1A modification. Furthermore, this review delves into the key players in m1A modification, known as the "writers," "erasers," and "readers." m1A modification is modified by the m1A methyltransferases, or writers, such as TRMT6, TRMT61A, TRMT61B, TRMT10C, NML, and, removed by the demethylases, or erasers, including FTO and ALKBH1, ALKBH3. It is recognized by m1A-binding proteins YTHDF1, TYHDF2, TYHDF3, and TYHDC1, also known as "readers". Additionally, we explore the intricate relationship between m1A modification and its regulators and their implications for the development and progression of specific types of cancer, we discuss how m1A modification can potentially facilitate the discovery of novel approaches for cancer diagnosis, treatment, and prognosis. Our summary of m1A methylated adenosine modification detection methods and regulatory mechanisms in various cancers provides useful insights for cancer diagnosis, treatment, and prognosis. Video Abstract.

Indexed as

NeoplasmsAlkB Homolog 1, Histone H2a DioxygenaseAlkB Homolog 3, Alpha-Ketoglutarate-Dependent DioxygenaseAlpha-Ketoglutarate-Dependent Dioxygenase FTOHumansMethylationMethyltransferasesRNAALKBH1 protein, humanALKBH3 protein, humanAlkB Homolog 1, Histone H2a DioxygenaseAlkB Homolog 3, Alpha-Ketoglutarate-Dependent DioxygenaseAlpha-Ketoglutarate-Dependent Dioxygenase FTOFTO protein, humanMethyltransferasesRNADetect methodErasersN1-methyladenosineReadersRegulation of cancerWriters

Identifiers

PMID38291517
PMCPMC10826226

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.