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天然药物成分诱导肿瘤铁死亡及其相关机制。

Natural medicinal ingredients induce tumor ferroptosis and related mechanisms.

机构信息

Department of Pharmacy, Clinical Pharmacy Center, Zhejiang Provincial People's Hospital, Affiliated People's Hospital of Hangzhou Medical College, Hangzhou 310014, China.

出版信息

Zhejiang Da Xue Xue Bao Yi Xue Ban. 2021 Oct 25;50(5):601-606. doi: 10.3724/zdxbyxb-2021-0198.

DOI:10.3724/zdxbyxb-2021-0198
PMID:34986533
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8732248/
Abstract

Ferroptosis is an iron-dependent programmed cell death characterized by reactive oxygen species-induced lipid peroxide accumulation, which is different from cell apoptosis, pyroptosis, necrosis or autophagy. Ferroptosis plays an important role in the regulation of tumorigenesis and tumor development. Recent studies have shown that natural medicinal ingredients can induce ferroptosis in tumor cells through glutathione (GSH)/glutathione peroxidase 4 (GPx4) pathway, iron metabolism, lipid metabolism or other mechanisms. It has been reported that more than 30 natural medicinal ingredients can induce ferroptosis in tumor cells with multiple pathways and multiple targets. This article reviews the current research progress on the antitumor effects of natural medicinal ingredients through inducing cell ferroptosis.

摘要

铁死亡是一种依赖于铁的程序性细胞死亡,其特征是活性氧诱导的脂质过氧化物积累,与细胞凋亡、细胞焦亡、坏死或自噬不同。铁死亡在肿瘤发生和发展的调控中发挥重要作用。最近的研究表明,天然药用成分可以通过谷胱甘肽(GSH)/谷胱甘肽过氧化物酶 4(GPx4)途径、铁代谢、脂质代谢或其他机制诱导肿瘤细胞发生铁死亡。据报道,超过 30 种天然药用成分可以通过多种途径和多个靶点诱导肿瘤细胞发生铁死亡。本文综述了通过诱导细胞铁死亡发挥抗肿瘤作用的天然药用成分的研究进展。

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Natural medicinal ingredients induce tumor ferroptosis and related mechanisms.天然药物成分诱导肿瘤铁死亡及其相关机制。
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引用本文的文献

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Prospects for Anti-Tumor Mechanism and Potential Clinical Application Based on Glutathione Peroxidase 4 Mediated Ferroptosis.基于谷胱甘肽过氧化物酶 4 介导的铁死亡的抗肿瘤机制及潜在临床应用前景。
Int J Mol Sci. 2023 Jan 13;24(2):1607. doi: 10.3390/ijms24021607.
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Network Pharmacology Identifies Therapeutic Targets and the Mechanisms of Glutathione Action in Ferroptosis Occurring in Oral Cancer.网络药理学确定口腔癌铁死亡中谷胱甘肽作用的治疗靶点及机制
Front Pharmacol. 2022 Mar 14;13:851540. doi: 10.3389/fphar.2022.851540. eCollection 2022.

本文引用的文献

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Shuganning injection, a traditional Chinese patent medicine, induces ferroptosis and suppresses tumor growth in triple-negative breast cancer cells.疏肝宁注射液,一种中药专利药物,可诱导三阴性乳腺癌细胞发生铁死亡并抑制肿瘤生长。
Phytomedicine. 2021 May;85:153551. doi: 10.1016/j.phymed.2021.153551. Epub 2021 Mar 18.
2
Induction of ferroptosis in human nasopharyngeal cancer cells by cucurbitacin B: molecular mechanism and therapeutic potential.葫芦素 B 诱导人鼻咽癌细胞发生铁死亡:分子机制与治疗潜能。
Cell Death Dis. 2021 Mar 4;12(3):237. doi: 10.1038/s41419-021-03516-y.
3
Identification of a new natural biflavonoids against breast cancer cells induced ferroptosis via the mitochondrial pathway.鉴定一种新的天然双黄酮类化合物,通过线粒体途径抑制乳腺癌细胞铁死亡。
Bioorg Chem. 2021 Apr;109:104744. doi: 10.1016/j.bioorg.2021.104744. Epub 2021 Feb 17.
4
Oleanolic acid inhibits cervical cancer Hela cell proliferation through modulation of the ACSL4 ferroptosis signaling pathway.齐墩果酸通过调节 ACSL4 铁死亡信号通路抑制宫颈癌 Hela 细胞增殖。
Biochem Biophys Res Commun. 2021 Mar 19;545:81-88. doi: 10.1016/j.bbrc.2021.01.028. Epub 2021 Feb 3.
5
Identification of a small molecule as inducer of ferroptosis and apoptosis through ubiquitination of GPX4 in triple negative breast cancer cells.通过三阴性乳腺癌细胞中谷胱甘肽过氧化物酶4(GPX4)的泛素化鉴定一种小分子作为铁死亡和凋亡的诱导剂
J Hematol Oncol. 2021 Jan 20;14(1):19. doi: 10.1186/s13045-020-01016-8.
6
EF24 induces ferroptosis in osteosarcoma cells through HMOX1.EF24 通过 HMOX1 诱导骨肉瘤细胞发生铁死亡。
Biomed Pharmacother. 2021 Apr;136:111202. doi: 10.1016/j.biopha.2020.111202. Epub 2021 Jan 14.
7
The Inhibitory Effect of 6-Gingerol on Ubiquitin-Specific Peptidase 14 Enhances Autophagy-Dependent Ferroptosis and Anti-Tumor and .6-姜酚对泛素特异性肽酶14的抑制作用增强自噬依赖性铁死亡及抗肿瘤作用。
Front Pharmacol. 2020 Nov 13;11:598555. doi: 10.3389/fphar.2020.598555. eCollection 2020.
8
Corrigendum to "IMCA Induces Ferroptosis Mediated by SLC7A11 through the AMPK/mTOR Pathway in Colorectal Cancer".《“IMCA 通过 AMPK/mTOR 途径诱导 SLC7A11 介导的结直肠癌铁死亡”的勘误》
Oxid Med Cell Longev. 2020 Oct 27;2020:6901472. doi: 10.1155/2020/6901472. eCollection 2020.
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