Evidence map›Paper›PMID 39751705›Full record

ArticleJournal of neuro-oncology2025

Mifepristone achieves tumor suppression and ferroptosis through PR/p53/HO1/GPX4 axis in meningioma cells.

Qin Dai, Jinfei Wei, Ziwei Li, Ting Li, Yenan Fang, Xinyu Li, Bingyan Shen, Qiqi Xie, Min Wang, Wencan Wu

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Article in Journal of neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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

3 citing papers in PubMed.

  1. 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

10 authors.

Qin Dai *National Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Jinfei Wei *National Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Ziwei Li *National Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Ting LiNational Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Yenan FangNational Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Xinyu LiNational Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Bingyan ShenNational Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Qiqi XieNational Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Min WangNational Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China. 18068520016@eye.ac.cn.
Wencan WuNational Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China. wuwencan@wmu.edu.cn.

Funding

National Natural Science Foundation of China 82000930Natural Science Foundation of Zhejiang Province, China LY22H120009the Eye Hospital of Wenzhou Medical University ZYQNYS 201901the National Key Research and Development Program of China 2021YFA110120the Science and Technology Plan Project of Wenzhou Municipality, China Y20210993
6 · The paper itself

Abstract

purposeThis study explores the effects of mifepristone on the proliferation, motility, and invasion of malignant and benign meningioma cells, aiming to identify mifepristone-sensitive types and investigate the underlying molecular mechanisms.

methodsIOMM-Lee and HBL-52 meningioma cells were treated with 0, vehicle control (VC), 5, 10, 20, 40, and 80 μM of mifepristone for 12, 24, 48, 72, and 96 h. Proliferation was assessed via CCK8 assay, while motility and invasion were measured using wound scratch and transwell assays. RNA sequencing and RT-PCR were used to analyze gene expression changes.

resultsMifepristone inhibited proliferation, motility, and invasion in both IOMM-Lee and HBL-52 cells in a dose- and time-dependent manner. RNA sequencing showed up-regulated genes significantly enriched in the ferroptosis pathway in both cell lines, confirmed by increased p53 and HO1 expression, decreased GPX4 expression, lipid peroxidation, Fe

conclusionMifepristone induces ferroptosis in meningioma cells via the PR/p53/HO1/GPX4 axis, suggesting its potential as a treatment for ferroptosis-sensitive meningiomas. It also supplies new clues regarding ferroptosis as a treatment entry point for meningiomas.

Indexed as

FerroptosisMeningeal NeoplasmsMeningiomaMifepristoneCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHeme Oxygenase-1HumansPhospholipid Hydroperoxide Glutathione PeroxidaseReceptors, ProgesteroneSignal TransductionTumor Suppressor Protein p53Heme Oxygenase-1HMOX1 protein, humanMifepristonePhospholipid Hydroperoxide Glutathione PeroxidaseReceptors, ProgesteroneTP53 protein, humanTumor Suppressor Protein p53FerroptosisMeningiomaMifepristoneProgesterone receptor

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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.