Evidence map›Paper›PMID 35977935›Full record

ArticleCell death & disease2022

m6A RNA methylation-mediated NDUFA4 promotes cell proliferation and metabolism in gastric cancer.

Weihong Xu, Yanan Lai, Yunqi Pan, Meiyu Tan, Yanyun Ma, Huiming Sheng, Jiucun Wang

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

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 83 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Weihong XuSchool of Life Sciences, Fudan University, Shanghai, 200433, China. xwh3066@126.com.ORCID 0000-0001-7569-7808
Yanan LaiDepartment of Clinical Laboratory, Shanghai Tongren Hospital, Shanghai, 200336, China.
Yunqi PanDepartment of Clinical Laboratory, Shanghai Tongren Hospital, Shanghai, 200336, China.
Meiyu TanDepartment of Clinical Laboratory, Shanghai Tongren Hospital, Shanghai, 200336, China.
Yanyun MaDepartment of Anthropology and Human Genetics, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Huiming ShengDepartment of Clinical Laboratory, Shanghai Tongren Hospital, Shanghai, 200336, China.
Jiucun WangSchool of Life Sciences, Fudan University, Shanghai, 200433, China. jcwang@fudan.edu.cn.ORCID 0000-0003-2765-0620
Tongren Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is a malignancy with poor prognosis. NDUFA4 is reported to correlate with the progression of GC. However, its underlying mechanism in GC is unknown. Our study was to reveal the pathogenic mechanism of NDUFA4 in GC. NDUFA4 expression was explored in single-cell and bulk RNA-seq data as well as GC tissue microarray. Mitochondrial respiration and glycolysis were estimated by oxygen consumption rate and extracellular acidification rate, respectively. The interaction between NDUFA4 and METTL3 was validated by RNA immunoprecipitation. Flow cytometry was used to estimate cell cycle, apoptosis and mitochondrial activities. NDUFA4 was highly expressed in GC and its high expression indicated a poor prognosis. The knockdown of NDUFA4 could reduce cell proliferation and inhibit tumor growth. Meanwhile, NDUFA4 could promote glycolytic and oxidative metabolism in GC cells, whereas the inhibition of glycolysis suppressed the proliferation and tumor growth of GC. Besides, NDUFA4 inhibited ROS level and promoted MMP level in GC cells, whereas the inhibition of mitochondrial fission could reverse NDUFA4-induced glycolytic and oxidative metabolism and tumor growth of GC. Additionally, METTL3 could increase the m6A level of NDUFA4 mRNA via the m6A reader IGF2BP1 to promote NDUFA4 expression in GC cells. Our study revealed that NDUFA4 was increased by m6A methylation and could promote GC development via enhancing cell glycolysis and mitochondrial fission. NDUFA4 was a potential target for GC treatment.

Indexed as

Stomach NeoplasmsCell Line, TumorCell ProliferationElectron Transport Complex IVGene Expression Regulation, NeoplasticHumansMethylationMethyltransferasesRNA, MessengerElectron Transport Complex IVMethyltransferasesMETTL3 protein, humanNDUFA4 protein, humanRNA, Messenger

Identifiers

PMID35977935
PMCPMC9385701
OpenAlexW4292113259

What OpenQuestion holds

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LicenceCC BY
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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.