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胶质瘤治疗中的铁死亡:现状、前景与药物应用

Ferroptosis in glioma treatment: Current situation, prospects and drug applications.

作者信息

Zhou Yuhang, Fang Chaoyou, Xu Houshi, Yuan Ling, Liu Yibo, Wang Xiaoyu, Zhang Anke, Shao Anwen, Zhou Danyang

机构信息

Health Management Center, Tongde Hospital of Zhejiang Province, Hangzhou, China.

The First Clinical Medical College, Heilongjiang University of Chinese Medicine, Harbin, China.

出版信息

Front Oncol. 2022 Sep 29;12:989896. doi: 10.3389/fonc.2022.989896. eCollection 2022.

DOI:10.3389/fonc.2022.989896
PMID:36249003
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9557197/
Abstract

Ferroptosis is a regulatory form of iron-dependent cell death caused by the accumulation of lipid-based reactive oxygen species (ROS) and differs from apoptosis, pyroptosis, and necrosis. Especially in neoplastic diseases, the susceptibility of tumor cells to ferroptosis affects prognosis and is associated with complex effects. Gliomas are the most common primary intracranial tumors, accounting for disease in 81% of patients with malignant brain tumors. An increasing number of studies have revealed the particular characteristics of iron metabolism in glioma cells. Therefore, agents that target a wide range of molecules involved in ferroptosis may regulate this process and enhance glioma treatment. Here, we review the underlying mechanisms of ferroptosis and summarize the potential therapeutic options for targeting ferroptosis in glioma.

摘要

铁死亡是一种由脂质活性氧(ROS)积累引起的铁依赖性细胞死亡的调控形式,与凋亡、焦亡和坏死不同。特别是在肿瘤性疾病中,肿瘤细胞对铁死亡的易感性影响预后,并与复杂的效应相关。胶质瘤是最常见的原发性颅内肿瘤,占恶性脑肿瘤患者的81%。越来越多的研究揭示了胶质瘤细胞中铁代谢的特殊特征。因此,靶向参与铁死亡的多种分子的药物可能调节这一过程并增强胶质瘤治疗效果。在此,我们综述铁死亡的潜在机制,并总结靶向胶质瘤中铁死亡的潜在治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82e2/9557197/69e109bcfe39/fonc-12-989896-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82e2/9557197/69e109bcfe39/fonc-12-989896-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82e2/9557197/69e109bcfe39/fonc-12-989896-g001.jpg

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本文引用的文献

1
The ubiquitin hydrolase OTUB1 promotes glioma cell stemness via suppressing ferroptosis through stabilizing SLC7A11 protein.泛素水解酶 OTUB1 通过稳定 SLC7A11 蛋白来抑制铁死亡从而促进神经胶质瘤细胞干性。
Bioengineered. 2021 Dec;12(2):12636-12645. doi: 10.1080/21655979.2021.2011633.
2
Downregulated Ferroptosis-Related Gene STEAP3 as a Novel Diagnostic and Prognostic Target for Hepatocellular Carcinoma and Its Roles in Immune Regulation.铁死亡相关基因STEAP3下调作为肝细胞癌的新型诊断和预后靶点及其在免疫调节中的作用
Front Cell Dev Biol. 2021 Nov 1;9:743046. doi: 10.3389/fcell.2021.743046. eCollection 2021.
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基于碳点的席夫碱的合成及其在胶质瘤细胞中的选择性抗癌活性。
RSC Adv. 2024 Jan 8;14(3):1952-1961. doi: 10.1039/d3ra06411e. eCollection 2024 Jan 3.
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Research progress on ferroptosis in gliomas (Review).胶质瘤中铁死亡的研究进展(综述)
Oncol Lett. 2023 Nov 27;27(1):36. doi: 10.3892/ol.2023.14169. eCollection 2024 Jan.
Chemical hybridization of sulfasalazine and dihydroartemisinin promotes brain tumor cell death.
柳氮磺胺吡啶和青蒿琥酯的化学杂交促进脑肿瘤细胞死亡。
Sci Rep. 2021 Oct 21;11(1):20766. doi: 10.1038/s41598-021-99960-z.
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Temozolomide Drives Ferroptosis via a DMT1-Dependent Pathway in Glioblastoma Cells.替莫唑胺通过 DMT1 依赖途径在胶质母细胞瘤细胞中诱导铁死亡。
Yonsei Med J. 2021 Sep;62(9):843-849. doi: 10.3349/ymj.2021.62.9.843.
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The Role of NCOA4-Mediated Ferritinophagy in Ferroptosis.NCOA4 介导线粒体铁蛋白自噬在铁死亡中的作用。
Adv Exp Med Biol. 2021;1301:41-57. doi: 10.1007/978-3-030-62026-4_4.
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Non-enzymatic lipid peroxidation initiated by photodynamic therapy drives a distinct ferroptosis-like cell death pathway.光动力学疗法引发的非酶脂质过氧化作用驱动了一种独特的类铁死亡细胞死亡途径。
Redox Biol. 2021 Sep;45:102056. doi: 10.1016/j.redox.2021.102056. Epub 2021 Jun 23.
7
Regulation of ferroptosis in cancer cells by YAP/TAZ and Hippo pathways: The therapeutic implications.YAP/TAZ和Hippo信号通路对癌细胞铁死亡的调控及其治疗意义
Genes Dis. 2020 May 18;8(3):241-249. doi: 10.1016/j.gendis.2020.05.004. eCollection 2021 May.
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Adaptive Changes Allow Targeting of Ferroptosis for Glioma Treatment.适应性变化可使铁死亡成为治疗脑胶质瘤的新靶点。
Cell Mol Neurobiol. 2022 Oct;42(7):2055-2074. doi: 10.1007/s10571-021-01092-5. Epub 2021 Apr 24.
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