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铁死亡的分子机制及其在胶质瘤进展和治疗中的作用。

The molecular mechanisms of ferroptosis and its role in glioma progression and treatment.

作者信息

Lu Mengyang, Zhou Yuanshuai, Sun Linjuan, Shafi Shaheryar, Ahmad Nafees, Sun Minxuan, Dong Jun

机构信息

Noncoding RNA and Cancer Lab, Faculty of Life Sciences, Shanghai University, Shanghai, China.

Jiangsu Key Laboratory of Medical Optics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, Suzhou, China.

出版信息

Front Oncol. 2022 Aug 16;12:917537. doi: 10.3389/fonc.2022.917537. eCollection 2022.

DOI:10.3389/fonc.2022.917537
PMID:36091118
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9450584/
Abstract

Ferroptosis is one of the programmed modes of cell death that has attracted widespread attention recently and is capable of influencing the developmental course and prognosis of many tumors. Glioma is one of the most common primary tumors of the central nervous system, but effective treatment options are very limited. Ferroptosis plays a critical role in the glioma progression, affecting tumor cell proliferation, angiogenesis, tumor necrosis, and shaping the immune-resistant tumor microenvironment. Inducing ferroptosis has emerged as an attractive strategy for glioma. In this paper, we review ferroptosis-related researches on glioma progression and treatment.

摘要

铁死亡是一种最近引起广泛关注的程序性细胞死亡模式,能够影响许多肿瘤的发展进程和预后。胶质瘤是中枢神经系统最常见的原发性肿瘤之一,但有效的治疗选择非常有限。铁死亡在胶质瘤进展中起关键作用,影响肿瘤细胞增殖、血管生成、肿瘤坏死,并塑造免疫抵抗性肿瘤微环境。诱导铁死亡已成为一种有吸引力的胶质瘤治疗策略。在本文中,我们综述了与胶质瘤进展和治疗相关的铁死亡研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da88/9450584/0ccd5207efe7/fonc-12-917537-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da88/9450584/34b2a45e7cf2/fonc-12-917537-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da88/9450584/0ccd5207efe7/fonc-12-917537-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da88/9450584/34b2a45e7cf2/fonc-12-917537-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da88/9450584/0ccd5207efe7/fonc-12-917537-g002.jpg

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本文引用的文献

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The critical role and molecular mechanisms of ferroptosis in antioxidant systems: a narrative review.铁死亡在抗氧化系统中的关键作用及分子机制:一篇叙述性综述
Ann Transl Med. 2022 Mar;10(6):368. doi: 10.21037/atm-21-6942.
2
The dual role of p62 in ferroptosis of glioblastoma according to p53 status.根据p53状态,p62在胶质母细胞瘤铁死亡中的双重作用。
Cell Biosci. 2022 Feb 25;12(1):20. doi: 10.1186/s13578-022-00764-z.
3
Ferroptosis, as the most enriched programmed cell death process in glioma, induces immunosuppression and immunotherapy resistance.
在U251胶质母细胞瘤细胞中调节增殖和侵袭的作用。 (原文“of”后面缺少具体内容)
Contemp Oncol (Pozn). 2025;29(2):195-205. doi: 10.5114/wo.2025.150649. Epub 2025 May 12.
4
Revisiting the potential of regulated cell death in glioma treatment: a focus on autophagy-dependent cell death, anoikis, ferroptosis, cuproptosis, pyroptosis, immunogenic cell death, and the crosstalk between them.重新审视调控性细胞死亡在胶质瘤治疗中的潜力:聚焦自噬依赖性细胞死亡、失巢凋亡、铁死亡、铜死亡、焦亡、免疫原性细胞死亡及其相互作用
Front Oncol. 2024 Aug 9;14:1397863. doi: 10.3389/fonc.2024.1397863. eCollection 2024.
5
Orexin-A mediates glioblastoma proliferation inhibition by increasing ferroptosis triggered by unstable iron pools and GPX4 depletion.食欲素-A 通过增加不稳定铁池和 GPX4 耗竭引发的铁死亡来抑制神经胶质瘤增殖。
J Cell Mol Med. 2024 May;28(9):e18318. doi: 10.1111/jcmm.18318.
6
Exosomal HSPB1, interacting with FUS protein, suppresses hypoxia-induced ferroptosis in pancreatic cancer by stabilizing Nrf2 mRNA and repressing P450.外泌体 HSPB1 与 FUS 蛋白相互作用,通过稳定 Nrf2 mRNA 和抑制 P450 来抑制胰腺癌缺氧诱导的铁死亡。
J Cell Mol Med. 2024 May;28(9):e18209. doi: 10.1111/jcmm.18209.
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Ferroptosis and its emerging role in kidney stone formation.铁死亡及其在肾结石形成中的新作用。
Mol Biol Rep. 2024 Feb 20;51(1):314. doi: 10.1007/s11033-024-09259-1.
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Impact of ferroptosis-related risk genes on macrophage M1/M2 polarization and prognosis in glioblastoma.铁死亡相关风险基因对胶质母细胞瘤中巨噬细胞M1/M2极化及预后的影响
Front Cell Neurosci. 2024 Jan 10;17:1294029. doi: 10.3389/fncel.2023.1294029. eCollection 2023.
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Front Genet. 2023 Jan 4;13:996180. doi: 10.3389/fgene.2022.996180. eCollection 2022.
铁死亡是胶质瘤中最丰富的程序性细胞死亡过程,它会诱导免疫抑制和免疫治疗抵抗。
Neuro Oncol. 2022 Jul 1;24(7):1113-1125. doi: 10.1093/neuonc/noac033.
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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。
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Hypoxia: The Cornerstone of Glioblastoma.缺氧:胶质母细胞瘤的基石。
Int J Mol Sci. 2021 Nov 22;22(22):12608. doi: 10.3390/ijms222212608.
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Ferroptosis Mediated by Lipid Reactive Oxygen Species: A Possible Causal Link of Neuroinflammation to Neurological Disorders.脂质活性氧物种介导的铁死亡:神经炎症与神经疾病关联的可能病因。
Oxid Med Cell Longev. 2021 Oct 23;2021:5005136. doi: 10.1155/2021/5005136. eCollection 2021.
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Over-expression of lncRNA TMEM161B-AS1 promotes the malignant biological behavior of glioma cells and the resistance to temozolomide via up-regulating the expression of multiple ferroptosis-related genes by sponging hsa-miR-27a-3p.lncRNA TMEM161B-AS1的过表达通过海绵化hsa-miR-27a-3p上调多个铁死亡相关基因的表达,从而促进胶质瘤细胞的恶性生物学行为和对替莫唑胺的耐药性。
Cell Death Discov. 2021 Oct 23;7(1):311. doi: 10.1038/s41420-021-00709-4.
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Versatile metal-phenolic network nanoparticles for multitargeted combination therapy and magnetic resonance tracing in glioblastoma.多功能金属-酚醛网络纳米颗粒用于胶质母细胞瘤的多靶点联合治疗和磁共振示踪。
Biomaterials. 2021 Nov;278:121163. doi: 10.1016/j.biomaterials.2021.121163. Epub 2021 Sep 28.
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Toward improved human health: Nrf2 plays a critical role in regulating ferroptosis.为了改善人类健康:Nrf2 在调节铁死亡方面发挥着关键作用。
Food Funct. 2021 Oct 19;12(20):9583-9606. doi: 10.1039/d1fo01036k.