Evidence map›Paper›PMID 36114749›Full record

ArticleCancer science2023

METTL3-mediated m6A mRNA contributes to the resistance of carbon-ion radiotherapy in non-small-cell lung cancer.

Xiaofeng Xu, Peiru Zhang, Yangle Huang, Weizhong Shi, Jingfang Mao, Ningyi Ma, Lin Kong, Lin Guo, Jinlong Liu, Jian Chen and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-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

32 citing papers in PubMed, 38 citations in OpenAlex.

  1. Targeting mDiscover oncology · 2026
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  8. Article
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  12. Article
  13. Article
  14. Review
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  16. The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024
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  17. Epitranscriptomic RNA mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
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  18. NClinical and translational medicine · 2024
    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

11 authors at 3 institutions in 1 country.

Xiaofeng XuDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Peiru ZhangDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.ORCID https://orcid.org/0000-0002-5896-8511
Yangle HuangDepartment of Radiation Oncology, Shanghai Engineering Research Center of Proton and Heavy Ion Radiation Therapy, Shanghai Proton and Heavy Ion Center, Shanghai, China.
Weizhong ShiDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Jingfang MaoDepartment of Radiation Oncology, Shanghai Engineering Research Center of Proton and Heavy Ion Radiation Therapy, Shanghai Proton and Heavy Ion Center, Shanghai, China.
Ningyi MaDepartment of Radiation Oncology, Shanghai Engineering Research Center of Proton and Heavy Ion Radiation Therapy, Shanghai Proton and Heavy Ion Center, Shanghai, China.
Lin KongDepartment of Radiation Oncology, Shanghai Engineering Research Center of Proton and Heavy Ion Radiation Therapy, Shanghai Proton and Heavy Ion Center, Shanghai, China.
Lin GuoDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.ORCID https://orcid.org/0000-0002-8419-3350
Jinlong LiuZhangjiang Institute, Fudan University, Shanghai, China.
Jian ChenDepartment of Radiation Oncology, Shanghai Engineering Research Center of Proton and Heavy Ion Radiation Therapy, Shanghai Proton and Heavy Ion Center, Shanghai, China.
Renquan LuDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Fudan University Shanghai Cancer Center · CNShanghai Genon Biological Products (China) · CNFudan University · CN

Funding

Science and Technology Development Fund of Shanghai Pudong New Area PKJ2017-Y53Shanghai Shen Kang Hospital Development Center New Frontier Technology Joint Project of Municipal Hospital SHDC12017114
6 · The paper itself

Abstract

Lung cancer is one of the leading causes of death among cancer patients worldwide. Carbon-ion radiotherapy is a radical nonsurgical treatment with high local control rates and no serious adverse events. N6-methyladenosine (m6A) modification is one of the most common chemical modifications in eukaryotic messenger RNA (mRNA) and has important effects on the stability, splicing, and translation of mRNAs. Recently, the regulatory role of m6A in tumorigenesis has been recognized more and more. However, the dysregulation of m6A and its role in carbon-ion radiotherapy of non-small-cell lung cancer (NSCLC) remains unclear. In this study, we found that the level of methyltransferase-like 3 (METTL3) and its mediated m6A modification were elevated in NSCLC cells with carbon-ion radiotherapy. Knockdown of METTL3 in NSCLC cells impaired proliferation, migration, and invasion in vitro and in vivo. Moreover, we found that METTL3-mediated m6A modification of mRNA inhibited the decay of H2A histone family member X (H2AX) mRNA and enhanced its expression, which led to enhanced DNA damage repair and cell survival.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsCarbonHumansMethyltransferasesRNA, MessengerCarbonMethyltransferasesMETTL3 protein, humanRNA, Messengercarbon-ion radiotherapyH2AXmethyltransferase-like 3N6-methyladenosinenon-small-cell lung cancer

Identifiers

PMID36114749
PMCPMC9807515
OpenAlexW4296120454

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.