Evidence map›Paper›PMID 36087219›Full record

ArticleHuman cell2022

METTL3 promotes m6A hypermethylation of RBM14 via YTHDF1 leading to the progression of hepatocellular carcinoma.

Jingyao Hu, Liang Yang, Xueqiang Peng, Minghuan Mao, Xiaodan Liu, Jianbo Song, Hangyu Li, Fu Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  10. DNA 5mC and RNA mInternational journal of molecular sciences · 2024
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  15. A positive feedback circuit between RN7SK snRNA and mMolecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  16. Review
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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

8 authors at 2 institutions in 1 country.

Jingyao HuThe Seventh Department of General Surgery, The Fourth Affiliated Hospital of China Medical University, No. 4, Donggu Road, Chonggu District, Shenyang, 110000, Liaoning, People's Republic of China.
Liang YangThe Third Department of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110000, Liaoning, People's Republic of China.
Xueqiang PengThe Third Department of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110000, Liaoning, People's Republic of China.
Minghuan MaoDepartment of Urology Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110000, Liaoning, People's Republic of China.
Xiaodan LiuThe Fifth Department of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110000, Liaoning, People's Republic of China.
Jianbo SongInterventional Department, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110000, Liaoning, People's Republic of China.
Hangyu LiThe Third Department of General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, 110000, Liaoning, People's Republic of China. lihangyu088@163.com.
Fu ChenThe Seventh Department of General Surgery, The Fourth Affiliated Hospital of China Medical University, No. 4, Donggu Road, Chonggu District, Shenyang, 110000, Liaoning, People's Republic of China. 20161047@cmu.edu.cn.
China Medical University · CNFourth Affiliated Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver is a well-known immunological organ with unique microenvironment. In normal conditions, the rich immune-infiltrating cells cooperate with non-parenchymal cells, such as Kupffer cells (KCs). The presence of liver immunosuppressive microenvironment underlines the importance to dissect this interaction to understand how this cross-talk promotes tumor growth in hepatocellular carcinoma (HCC). Therefore, the aim of the study here was to probe the role of methyltransferase-like 3 (METTL3) in the HCC progression and its effect on the polarization of KCs. KCs showed M2 polarization, and METTL3 was overexpressed in our collected HCC tissues relative to adjacent tissues. METTL3 depletion inhibited the M2 polarization of KCs, thereby reverting the malignant phenotype of HCC cells in vitro and growth and metastasis in vivo. Mechanistically, YTH domain-containing family protein 1 (YTHDF1) bound to RNA-binding protein 14 (RBM14), whereas METTL3 knockdown in KCs cells suppressed RBM14 expression by decreasing N-methyladenosine (m6A) methylation. Overexpression of RBM14 mitigated the anti-tumor effects of sh-METTL3 in vitro and in vivo. It is suggested that the mechanism of sh-METTL3 suppressing the polarization of KCs and the progression of HCC is to regulate the RBM14 expression via YTHDF1-dependent m6A modification.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAdenosineDNA MethylationHumansIntracellular Signaling Peptides and ProteinsMethyltransferasesRNA-Binding ProteinsTumor MicroenvironmentAdenosineIntracellular Signaling Peptides and ProteinsMethyltransferasesMETTL3 protein, humanRBM14 protein, humanRNA-Binding ProteinsYTHDF1 protein, humanHepatocellular carcinomaKupffer cellsm6A modificationMETTL3RBM14

Identifiers

PMID36087219
OpenAlexW4296266930

What OpenQuestion holds

Textmetadata
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.