Evidence map›Paper›PMID 35784761›Full record

ReviewFrontiers in pharmacology2022

The Role of m6A RNA Methylation in Cancer: Implication for Nature Products Anti-Cancer Research.

Na Song, Kai Cui, Ke Zhang, Jie Yang, Jia Liu, Zhuang Miao, Feiyue Zhao, Hongjing Meng, Lu Chen, Chong Chen and 4 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
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

34 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. METTL16-mediated mJournal of experimental & clinical cancer research : CR · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Deciphering the role ofWorld journal of hepatology · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. m6A: a novel strategy for osteoporosis treatment.Frontiers in cell and developmental biology · 2025
    Review
  16. Targeting DTX2/UFD1-mediated FTO degradation to regulate antitumor immunity.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  17. Article
  18. Article
  19. Review
  20. mMedComm · 2024
    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

14 authors at 2 institutions in 1 country.

Na SongDepartment of Pathology, Key Laboratory of Clinical Molecular Pathology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Kai CuiDepartment of Pathology, Xinxiang Medical University, Xinxiang, China.
Ke ZhangDepartment of Pathology, Xinxiang Medical University, Xinxiang, China.
Jie YangDepartment of Pathology, Xinxiang Medical University, Xinxiang, China.
Jia LiuDepartment of Pathology, Xinxiang Medical University, Xinxiang, China.
Zhuang MiaoDepartment of Pathology, Xinxiang Medical University, Xinxiang, China.
Feiyue ZhaoDepartment of Pathology, Xinxiang Medical University, Xinxiang, China.
Hongjing MengDepartment of Pathology, Xinxiang Medical University, Xinxiang, China.
Lu ChenDepartment of Pathology, Xinxiang Medical University, Xinxiang, China.
Chong ChenDepartment of Pathology, Xinxiang Medical University, Xinxiang, China.
Yushan LiSchool of Public Health, Xinxiang Medical University, Xinxiang, China.
Minglong ShaoThe Second Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Jinghang ZhangDepartment of Pathology, Key Laboratory of Clinical Molecular Pathology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Haijun WangDepartment of Pathology, Key Laboratory of Clinical Molecular Pathology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Xinxiang Medical University · CNFirst Affiliated Hospital of Xinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

N6-methyladenosine (m6A) RNA methylation is identified as the most common, abundant and reversible RNA epigenetic modification in messenger RNA (mRNA) and non-coding RNA, especially within eukaryotic messenger RNAs (mRNAs), which post-transcriptionally directs many important processes of RNA. It has also been demonstrated that m6A modification plays a pivotal role in the occurrence and development of tumors by regulating RNA splicing, localization, translation, stabilization and decay. Growing number of studies have indicated that natural products have outstanding anti-cancer effects of their unique advantages of high efficiency and minimal side effects. However, at present, there are very few research articles to study and explore the relationship between natural products and m6A RNA modification in tumorigenesis. m6A is dynamically deposited, removed, and recognized by m6A methyltransferases (METTL3/14, METTL16, WTAP, RBM15/15B, VIRMA, CBLL1, and ZC3H13, called as "writers"), demethylases (FTO and ALKBH5, called as "erasers"), and m6A-specific binding proteins (YTHDF1/2/3, YTHDC1/2, IGH2BP1/2/3, hnRNPs, eIF3, and FMR1, called as "readers"), respectively. In this review, we summarize the biological function of m6A modification, the role of m6A and the related signaling pathway in cancer, such as AKT, NF-kB, MAPK, ERK, Wnt/β-catenin, STAT, p53, Notch signaling pathway, and so on. Furthermore, we reviewed the current research on nature products in anti-tumor, and further to get a better understanding of the anti-tumor mechanism, thus provide an implication for nature products with anti-cancer research by regulating m6A modification in the future.

Indexed as

anti-cancerimplicationm6Amolecular functionnature productsRNA methylationsignaling pathway

Identifiers

PMID35784761
PMCPMC9243580
OpenAlexW4283032810

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.