Evidence map›Paper›PMID 32452511›Full record

ArticleBioscience reports2020

Dihydroartemisinin initiates ferroptosis in glioblastoma through GPX4 inhibition.

Renxin Yi, Handong Wang, Chulei Deng, Xinyue Wang, Lei Yao, Wenhao Niu, Maoxing Fei, Wangdui Zhaba

Abstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 3 pooled it
–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

79 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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  9. Ferroptosis-induced immune modulation: a new frontier in glioblastoma therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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19 more citing papers are in PubMed but not listed here.

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.

Renxin YiDepartment of Neurosurgery, Jinling Hospital, Southeast University, School of Medicine, Nanjing 210002, P.R. China.
Handong WangDepartment of Neurosurgery, Jinling Hospital, Nanjing University, School of Medicine, Nanjing 210002, P.R. China.
Chulei DengDepartment of Neurosurgery, Jinling Hospital, South Medical University, School of Medicine, Nanjing 210002, P.R. China.
Xinyue WangState Key Laboratory of Bioelectronics, Jiangsu Laboratory for Biomaterials and Devices, School of Biological Science and Medical Engineering, Southeast University, Nanjing 210002, P.R. China.
Lei YaoDepartment of Neurosurgery, Jinling Hospital, Southeast University, School of Medicine, Nanjing 210002, P.R. China.
Wenhao NiuDepartment of Neurosurgery, Jinling Hospital, Southeast University, School of Medicine, Nanjing 210002, P.R. China.
Maoxing FeiDepartment of Neurosurgery, Jinling Hospital, Nanjing Medical University, School of Medicine, Nanjing 210002, P.R. China.
Wangdui ZhabaDepartment of Neurosurgery, Jinling Hospital, Nanjing University, School of Medicine, Nanjing 210002, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been demonstrated from previous studies about the killing effect of dihydroartemisinin (DHA) on glioblastoma, which involves multiple aspects: cytotoxicity, cell cycle arrest and invasion inhibition. DHA has the advantages of low cytotoxicity to normal cells, selective killing effect and low drug resistance, making it one of the popular anti-tumor research directions. Ferroptosis is a newly discovered form of cell death characterized by iron dependence and lipid reactive oxygen species (ROS) accumulation. In the present study, we found differences in the expression of transferrin receptors in normal human astrocytes (NHA) and glioblastoma cells (U87 and A172), which may be one of the mechanisms of DHA selective killing effect. Through the determination of ferroptosis-related protein expression, we found that the significant decrease of GPX4, accompanied by the constant expression of xCT and ACSL4, suggesting GPX4 was a pivotal target for DHA-activated ferroptosis in glioblastoma. Total and lipid ROS levels were increased and all these results could be reversed by the ferroptosis inhibitor, ferrostatin-1. These findings demonstrated ferroptosis would be a critical component of cell death caused by DHA and GPX4 was the main target. All these results provide a novel treatment direction to glioblastoma. The association between ferroptosis and polyamines is also discussed, which will provide new research directions for ferroptosis caused by DHA in glioblastoma.

Indexed as

Antineoplastic Agents, PhytogenicArtemisininsBrain NeoplasmsCell Line, TumorEnzyme InhibitorsFerroptosisGlioblastomaHumansPhospholipid Hydroperoxide Glutathione PeroxidaseReactive Oxygen SpeciesReceptors, TransferrinSignal TransductionAntineoplastic Agents, PhytogenicArtemisininsartenimolEnzyme InhibitorsPhospholipid Hydroperoxide Glutathione PeroxidaseReactive Oxygen SpeciesReceptors, Transferrindihydroartemisininferroptosisgliomaselectivetransferrin receptors

Identifiers

PMID32452511
PMCPMC7313443

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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.