Evidence map›Paper›PMID 34427071›Full record

ArticleYonsei medical journal2021

Temozolomide Drives Ferroptosis via a DMT1-Dependent Pathway in Glioblastoma Cells.

Qingxin Song, Shanxin Peng, Zhiqing Sun, Xueyuan Heng, Xiaosong Zhu

Open access · goldAbstract read
In one paragraph

Article in Yonsei medical journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 2 pooled it
11.9field-weighted citation impact, top 1% 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

76 citing papers in PubMed, 2 syntheses or guidelines pooled it, 114 citations in OpenAlex.

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  8. Ferroptosis-induced immune modulation: a new frontier in glioblastoma therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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16 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

5 authors at 2 institutions in 1 country.

Qingxin SongDepartment of Neurosurgery, Linyi People's Hospital, Shandong University, Linyi, Shandong, China.ORCID https://orcid.org/0000-0001-7339-8564
Shanxin PengDepartment of Infection Management, Linyi People's Hospital, Shandong University, Linyi, Shandong, China.ORCID https://orcid.org/0000-0002-8958-9370
Zhiqing SunDepartment of Neurology, Linyi People's Hospital, Shandong University, Linyi, Shandong, China.ORCID https://orcid.org/0000-0003-1730-3983
Xueyuan HengDepartment of Neurosurgery, Linyi People's Hospital, Shandong University, Linyi, Shandong, China. xueyuanheng@yahoo.com.ORCID https://orcid.org/0000-0002-8174-0347
Xiaosong ZhuDepartment of Infection Management, Linyi People's Hospital, Shandong University, Linyi, Shandong, China.ORCID https://orcid.org/0000-0001-9604-0792
Shandong University · CNLinyi People's Hospital · CN

Funding

Medical Health Science and Technology Development Plan of Shandong Province 2019WS134National Natural Science Foundation of China 82003435Natural Science Foundation of Shandong Province ZR2020QH332
6 · The paper itself

Abstract

purposeTemozolomide is used in first-line treatment for glioblastoma. However, chemoresistance to temozolomide is common in glioma patients. In addition, mechanisms for the anti-tumor effects of temozolomide are largely unknown. Ferroptosis is a form of programmed cell death triggered by disturbed redox homeostasis, overloaded iron, and increased lipid peroxidation. The present study was performed to elucidate the involvement of ferroptosis in the anti-tumor mechanisms of temozolomide. MATERIALS AND

methodsWe utilized the CCK8 assay to evaluate cytotoxicity. Levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), iron, and glutathione (GSH) were measured. Flow cytometry and fluorescence microscope were used to detect the production of reactive oxygen species (ROS). Western blotting, RT-PCR and siRNA transfection were used to investigate molecular mechanisms.

resultsTemozolomide increased the levels of LDH, MDA, and iron and reduced GSH levels in TG905 cells. Furthermore, we found that ROS levels and DMT1 expression were elevated in TG905 cells treated with temozolomide and were accompanied by a decrease in the expression of glutathione peroxidase 4, indicating an iron-dependent cell death, ferroptosis. Our results also showed that temozolomide-induced ferroptosis is associated with regulation of the Nrf2/HO-1 pathway. Conversely, DMT1 knockdown by siRNA evidently blocked temozolomide-induced ferroptosis in TG905 cells.

conclusionTaken together, our findings indicate that temozolomide may suppress cell growth partly by inducing ferroptosis by targeting DMT1 expression in glioblastoma cells.

Indexed as

FerroptosisGlioblastomaHumansLipid PeroxidationReactive Oxygen SpeciesTemozolomideReactive Oxygen SpeciesTemozolomideDMT1ferroptosisglioblastomareactive oxygen speciesTemozolomide

Identifiers

PMID34427071
PMCPMC8382730
OpenAlexW3195306241

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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.