Evidence map›Paper›PMID 41137882›Full record

ArticleCellular and molecular life sciences : CMLS2025

Mechanism of LncRNA NORAD regulating ferroptosis in endometrial cancer cells by modifying GPX4 through FTO-mediated m6A methylation.

Jieqi Ke, Ting Gao, Zhen Shen, Min Li, Tianjiao Zhang, Dabao Wu

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PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

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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

5 citing papers in PubMed.

  1. P53 Competitively Binds P300 to Suppress HIF-1α/TFRC-Mediated Ferroptosis and Promote Doxorubicin Resistance in Breast Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

6 authors.

Jieqi KeDepartment of Obstetrics and Gynecology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, No.9 Lujiang Road, Hefei, 230001, Anhui, P.R. China.
Ting GaoDepartment of Obstetrics and Gynecology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, No.9 Lujiang Road, Hefei, 230001, Anhui, P.R. China.
Zhen ShenDepartment of Obstetrics and Gynecology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, No.9 Lujiang Road, Hefei, 230001, Anhui, P.R. China.
Min LiDepartment of Obstetrics and Gynecology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, No.9 Lujiang Road, Hefei, 230001, Anhui, P.R. China.
Tianjiao ZhangDepartment of Obstetrics and Gynecology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, No.9 Lujiang Road, Hefei, 230001, Anhui, P.R. China.
Dabao WuDepartment of Obstetrics and Gynecology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, No.9 Lujiang Road, Hefei, 230001, Anhui, P.R. China. DabaoWu0118@163.com.ORCID http://orcid.org/0009-0005-9650-1604

Funding

Anhui Province Natural Science Foundation youth project 1808085QH274
6 · The paper itself

Abstract

objectiveEndometrial cancer (EC) represents the most prevalent gynecologic malignancy. We probed the mechanism of long noncoding RNA activated by DNA damage (lncRNA NORAD) regulating ferroptosis in EC cells (ECCs) by modifying glutathione peroxidase 4 (GPX4) through N6 methyladenosine (m6A) methylation.

methodsThe relationship between NORAD and EC clinically, and correlations of NORAD with GPX4 and fat mass and obesity-associated protein (FTO) levels were analyzed by Starbase database, Kaplan-Meier curve, and Pearson. Total m6A modification of EC tissues was detected by Dot blotting. Effects of regulating NORAD, GPX4, FTO and YTHDF2 on m6A modification and ferroptosis in EC were explored in ECCs and nude mouse xenograft tumor models. Mechanistically, NORAD-FTO, FTO-YTHDF2 and YTHDF2-GPX4 interactions were detected by RNA pull down, Co-IP and RIP assays. GPX4 mRNA stability was determined by Actinomycin D test.

resultsNORAD was down-regulated in EC tissues and cells. Lowly-expressed NORAD in EC tissues predicted EC patients' poor prognoses, and negatively correlated with GPX4. NORAD overexpression promoted GPX4-mediated ferroptosis. NORAD promoted ECC ferroptosis by down-regulating GPX4. NORAD promoted YTHDF2-mediated m6A modification to reduce GPX4 mRNA stability by interacting with FTO. YTHDF2 silencing or FTO overexpression partially averted NORAD-promoted ECC ferroptosis by modulating GPX4. NORAD promoted m6A modification to down-regulate GPX4 by interacting with FTO, and promoted ferroptosis to inhibit tumor growth in vivo.

conclusionNORAD was down-regulated in EC and affected the EC prognosis. NORAD overexpression facilitated YTHDF2-mediated m6A modification by interacting with FTO to elevate GPX4 degradation, thereby stimulating ECC ferroptosis and hindering EC progression.

Indexed as

AdenosineAlpha-Ketoglutarate-Dependent Dioxygenase FTOEndometrial NeoplasmsFerroptosisPhospholipid Hydroperoxide Glutathione PeroxidaseRNA, Long NoncodingAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMethylationMiceMice, Inbred BALB CMice, NudeRNA-Binding ProteinsAdenosineAlpha-Ketoglutarate-Dependent Dioxygenase FTOFTO protein, humanN-methyladenosineNORAD long non-coding RNA, humanPhospholipid Hydroperoxide Glutathione PeroxidaseRNA-Binding ProteinsRNA, Long NoncodingYTHDF2 protein, humanEndometrial cancer cellsFerroptosisFTOGPX4Long noncoding RNA NORADM6AMethylation modificationYTHDF2

Identifiers

PMID41137882
PMCPMC12553841

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LicenceCC BY-NC-ND
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Registered trials

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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.