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铁死亡:一种胶质瘤治疗的新策略及作用机制

Ferroptosis: A novel therapeutic strategy and mechanism of action in glioma.

作者信息

Zhang Gaosen, Fang Yi, Li Xiang, Zhang Zhen

机构信息

Department of Ultrasound, First Affiliated Hospital of China Medical University, Shenyang, China.

出版信息

Front Oncol. 2022 Sep 15;12:947530. doi: 10.3389/fonc.2022.947530. eCollection 2022.

DOI:10.3389/fonc.2022.947530
PMID:36185243
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9520297/
Abstract

Glioma is the most common malignant tumor of the central nervous system and resistance is easily developed to chemotherapy drugs during the treatment process, resulting in high mortality and short survival in glioma patients. Novel therapeutic approaches are urgently needed to improve the therapeutic efficacy of chemotherapeutic drugs and to improve the prognosis of patients with glioma. Ferroptosis is a novel regulatory cell death mechanism that plays a key role in cancer, neurodegenerative diseases, and other diseases. Studies have found that ferroptosis-related regulators are closely related to the survival of patients with glioma, and induction of ferroptosis can improve glioma resistance to chemotherapy drugs. Therefore, induction of tumor cell ferroptosis may be an effective therapeutic strategy for glioma. This review summarizes the relevant mechanisms of ferroptosis, systematically summarizes the key role of ferroptosis in the treatment of glioma and outlines the relationship between ferroptosis-related ncRNAs and the progression of glioma.

摘要

胶质瘤是中枢神经系统最常见的恶性肿瘤,在治疗过程中很容易对化疗药物产生耐药性,导致胶质瘤患者死亡率高、生存期短。迫切需要新的治疗方法来提高化疗药物的治疗效果,并改善胶质瘤患者的预后。铁死亡是一种新型的调节性细胞死亡机制,在癌症、神经退行性疾病和其他疾病中起关键作用。研究发现,铁死亡相关调节因子与胶质瘤患者的生存密切相关,诱导铁死亡可提高胶质瘤对化疗药物的耐药性。因此,诱导肿瘤细胞铁死亡可能是治疗胶质瘤的一种有效策略。本文综述了铁死亡的相关机制,系统总结了铁死亡在胶质瘤治疗中的关键作用,并概述了铁死亡相关非编码RNA与胶质瘤进展之间的关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd9c/9520297/945fab2e948b/fonc-12-947530-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd9c/9520297/00507f6e2ee3/fonc-12-947530-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd9c/9520297/945fab2e948b/fonc-12-947530-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd9c/9520297/00507f6e2ee3/fonc-12-947530-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd9c/9520297/945fab2e948b/fonc-12-947530-g002.jpg

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本文引用的文献

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Molecules. 2022 May 7;27(9):3011. doi: 10.3390/molecules27093011.
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Glioblastoma Relapses Show Increased Markers of Vulnerability to Ferroptosis.胶质母细胞瘤复发显示出对铁死亡易感性增加的标志物。
Front Oncol. 2022 Apr 21;12:841418. doi: 10.3389/fonc.2022.841418. eCollection 2022.
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LINC01564 Promotes the TMZ Resistance of Glioma Cells by Upregulating NFE2L2 Expression to Inhibit Ferroptosis.
非编码RNA:铁死亡谷胱甘肽-GPX4途径中的关键调节因子。
Noncoding RNA Res. 2024 May 20;9(4):1222-1234. doi: 10.1016/j.ncrna.2024.05.007. eCollection 2024 Dec.
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High Expression of in the Prognosis of Glioma and Its Relationship with Ferroptosis and Immunity.在胶质瘤预后中的高表达及其与铁死亡和免疫的关系。
Genes (Basel). 2023 Jul 6;14(7):1406. doi: 10.3390/genes14071406.
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High-Dose Selenium Induces Ferroptotic Cell Death in Ovarian Cancer.高剂量硒诱导卵巢癌细胞发生铁死亡。
Int J Mol Sci. 2023 Jan 18;24(3):1918. doi: 10.3390/ijms24031918.
LINC01564 通过上调 NFE2L2 表达抑制铁死亡促进胶质瘤细胞 TMZ 耐药性。
Mol Neurobiol. 2022 Jun;59(6):3829-3844. doi: 10.1007/s12035-022-02736-3. Epub 2022 Apr 14.
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Targeting NQO1/GPX4-mediated ferroptosis by plumbagin suppresses in vitro and in vivo glioma growth.通过白花丹醌靶向 NQO1/GPX4 介导的铁死亡抑制体外和体内神经胶质瘤生长。
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