Evidence map›Paper›PMID 39863603›Full record

ArticleCell death discovery2025

IDO1 inhibits ferroptosis by regulating FTO-mediated m6A methylation and SLC7A11 mRNA stability during glioblastoma progression.

Qianting Tian, Guixue Dan, Xuyan Wang, Jiamei Zhu, Chaochun Chen, Dekun Tang, Ziming Wang, Dan Chen, Shan Lei, Chao Yang and 5 more

Abstract read
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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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

15 authors.

Qianting Tian *Department of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.ORCID http://orcid.org/0009-0000-0913-5305
Guixue Dan *Department of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.ORCID http://orcid.org/0009-0005-1003-9069
Xuyan Wang *Department of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.
Jiamei ZhuDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.
Chaochun ChenDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.
Dekun TangDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.
Ziming WangDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.
Dan ChenDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.
Shan LeiDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.
Chao YangState Key Laboratory of Functions and Applications of Medicinal Plants, School of Basic Medical Sciences, Guizhou Provincial Engineering Technology Research Center for Chemical Drug R&D, Guizhou Medical University, Guiyang, China.
Houmei WangDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.
Bing GuoDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China.ORCID http://orcid.org/0000-0001-8998-2597
Bangming JinDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China. BMJin@gmc.edu.cn.ORCID http://orcid.org/0000-0002-2997-5587
Tengxiang ChenDepartment of Physiology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, China. txch@gmc.edu.cn.ORCID http://orcid.org/0000-0001-6907-1374
Lei TangState Key Laboratory of Functions and Applications of Medicinal Plants, School of Basic Medical Sciences, Guizhou Provincial Engineering Technology Research Center for Chemical Drug R&D, Guizhou Medical University, Guiyang, China. tlei1974@163.com.ORCID http://orcid.org/0000-0003-1771-3878

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Indoleamine 2, 3-dioxygenase 1 (IDO1) has been recognized as an enzyme involved in tryptophan catabolism with immunosuppressive ability. This study determined to investigate the impact of IDO1 on glioblastoma multiforme (GBM) cells. Here, we showed that the expression of IDO1 was markedly increased in patients with glioma and associated with GBM progression. IDO1 overexpression suppressed ferroptotic cell death, reduced ROS and lipid peroxide generation in GBM cells. IDO1 expression increased the SLC7A11 mRNA stability through FTO-dependent m6A methylation. Mechanistically, IDO1 promoted the AhR expression and nuclear translocation, thus facilitating AhR recruitment at the promoter regions of FTO gene and negatively regulating its transcription. These findings demonstrate that IDO1 facilitates GBM progression by inhibiting SLC7A11-dependent ferroptosis through an IDO1-AhR-FTO axis-mediated m6A methylation mechanism.

Identifiers

PMID39863603
PMCPMC11762296

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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.