Evidence map›Paper›PMID 39666195›Full record

ArticleNeuroscience bulletin2025

Dysregulation of Iron Homeostasis Mediated by FTH Increases Ferroptosis Sensitivity in TP53-Mutant Glioblastoma.

Xuejie Huan, Jiangang Li, Zhaobin Chu, Hongliang Zhang, Lei Cheng, Peng Lun, Xixun Du, Xi Chen, Qian Jiao, Hong Jiang

Abstract read
In one paragraph

Article in Neuroscience bulletin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Stereoelectroencephalography (SEEG)-guided insula resections: is it "Reily" worth it?Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024
    Article
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.

Xuejie HuanDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao, 266071, China.
Jiangang LiDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao, 266071, China.
Zhaobin ChuCollege of Life Sciences, University of Chinese Academy of Sciences, Beijing, 101408, China.
Hongliang ZhangDepartment of Neurosurgery, the Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Lei ChengDepartment of Neurosurgery, the Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Peng LunDepartment of Neurosurgery, the Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Xixun DuDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao, 266071, China.
Xi ChenDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao, 266071, China.
Qian JiaoDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao, 266071, China. jiaoqian@qdu.edu.cn.ORCID http://orcid.org/0000-0002-9716-4698
Hong JiangDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao, 266071, China. jianghong@uor.edu.cn.ORCID http://orcid.org/0000-0003-1524-7519

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron metabolism is a critical factor in tumorigenesis and development. Although TP53 mutations are prevalent in glioblastoma (GBM), the mechanisms by which TP53 regulates iron metabolism remain elusive. We reveal an imbalance iron homeostasis in GBM via TCGA database analysis. TP53 mutations disrupted iron homeostasis in GBM, characterized by elevated total iron levels and reduced ferritin (FTH). The gain-of-function effect triggered by TP53 mutations upregulates itchy E3 ubiquitin-protein ligase (ITCH) protein expression in astrocytes, leading to FTH degradation and an increase in free iron levels. TP53-mut astrocytes were more tolerant to the high iron environment induced by exogenous ferric ammonium citrate (FAC), but the increase in intracellular free iron made them more sensitive to Erastin-induced ferroptosis. Interestingly, we found that Erastin combined with FAC treatment significantly increased ferroptosis. These findings provide new insights for drug development and therapeutic modalities for GBM patients with TP53 mutations from iron metabolism perspectives.

Indexed as

Brain NeoplasmsFerritinsFerroptosisGlioblastomaHomeostasisIronTumor Suppressor Protein p53AstrocytesCell Line, TumorFerric CompoundsHumansMutationPiperazinesQuaternary Ammonium Compoundserastinferric ammonium citrateFerric CompoundsFerritinsIronPiperazinesQuaternary Ammonium CompoundsTP53 protein, humanTumor Suppressor Protein p53ErastinFerroptosisGlioblastomaIron metabolismTP53 mutation

Identifiers

PMID39666195
PMCPMC11978602

What OpenQuestion holds

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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.