Evidence map›Paper›PMID 38084791›Full record

ArticleCell proliferation2024

METTL16-mediated N6-methyladenosine modification of Soga1 enables proper chromosome segregation and chromosomal stability in colorectal cancer.

Jimin Li, Fang Yang, Zeyu Wang, Siqing Zheng, Shuang Zhang, Chen Wang, Bing He, Jia-Bei Wang, Hao Wang

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 15 citations in OpenAlex.

  1. METTL16 promotes colorectal cancer progression and CD8Medical oncology (Northwood, London, England) · 2026
    Article
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  3. Review
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  5. Review
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  13. METTL Family in Healthy and Disease.Molecular biomedicine · 2024
    Review
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  16. 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

9 authors at 4 institutions in 1 country.

Jimin LiDepartment of Laboratory Medicine, The Affiliated Anhui Provincial Hospital of Anhui Medical University, Hefei, China.
Fang YangDepartment of Clinical Laboratory, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, China.
Zeyu WangGraduate School, Bengbu Medical College, Bengbu, China.
Siqing ZhengSchool of Pharmacy, Anhui Medical University, Hefei, China.
Shuang ZhangDepartment of Laboratory Medicine, The Affiliated Anhui Provincial Hospital of Anhui Medical University, Hefei, China.
Chen WangDepartment of Laboratory Medicine, The Affiliated Anhui Provincial Hospital of Anhui Medical University, Hefei, China.
Bing HeDepartment of Laboratory Medicine, The Affiliated Anhui Provincial Hospital of Anhui Medical University, Hefei, China.
Jia-Bei WangDepartment of Hepatobiliary Surgery, Anhui Province Key Laboratory of Hepatopancreatobiliary Surgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Heifei, China.
Hao WangDepartment of Laboratory Medicine, The Affiliated Anhui Provincial Hospital of Anhui Medical University, Hefei, China.ORCID https://orcid.org/0000-0003-4807-3172
Anhui Medical University · CNBengbu Medical College · CNUniversity of Science and Technology of China · CNWannan Medical College · CN

Funding

Natural Science Foundation of Anhui Province 2008085MH241Scientific Research Project of Anhui Provincial Education Department 2022AH020079
6 · The paper itself

Abstract

N6-methyladenosine (m6A) is the most prevalent internal modification in mammalian messenger RNAs and is associated with numerous biological processes. However, its role in chromosomal instability remains to be established. Here, we report that an RNA m6A methyltransferase, METTL16, plays an indispensable role in the progression of chromosome segregation and is required to preserve chromosome stability in colorectal cancer (CRC) cells. Depletion or inhibition of the methyltransferase activity of METTL16 results in abnormal kinetochore-microtubule attachment during mitosis, leading to delayed mitosis, lagging chromosomes, chromosome mis-segregation and chromosomal instability. Mechanistically, METTL16 exerts its oncogenic effects by enhancing the expression of suppressor of glucose by autophagy 1 (Soga1) in an m6A-dependent manner. CDK1 phosphorylates Soga1, thereby triggering its direct interaction with the polo box domain of PLK1. This interaction facilitates PLK1 activation and promotes mitotic progression. Therefore, targeting the METTL16-Soga1 pathway may provide a potential treatment strategy against CRC because of its essential role in maintaining chromosomal stability.

Indexed as

AdenosineChromosomal InstabilityChromosome SegregationColorectal NeoplasmsIntracellular Signaling Peptides and ProteinsMethyltransferasesAnimalsCDC2 Protein KinaseCell Line, TumorHumansMiceMitosisPolo-Like Kinase 1Protein Serine-Threonine KinasesAdenosineCDC2 Protein KinaseIntracellular Signaling Peptides and ProteinsMethyltransferasesMETTL16 protein, humanN-methyladenosinePolo-Like Kinase 1Protein Serine-Threonine KinasesSOGA1 protein, human

Identifiers

PMID38084791
PMCPMC11056707
OpenAlexW4389607247

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.