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铁死亡:膀胱癌的新治疗靶点。

Ferroptosis: A new therapeutic target for bladder cancer.

作者信息

Zeng Fan, Lan Yunping, Wang Ning, Huang Xiaobo, Zhou Qiao, Wang Yi

机构信息

Department of Critical Care Medicine, Sichuan Academy of Medical Science, Chengdu, China.

Department of Rheumatology and Immunology, Sichuan Academy of Medical Science and Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.

出版信息

Front Pharmacol. 2022 Nov 3;13:1043283. doi: 10.3389/fphar.2022.1043283. eCollection 2022.

DOI:10.3389/fphar.2022.1043283
PMID:36408230
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9669411/
Abstract

Bladder cancer (BC) is the most frequent type of urinary system cancer. The prognosis of BC is poor due to high metastasis rates and multidrug resistance. Hence, development of novel therapies targeting BC cell death is urgently needed. As a novel cell death type with strong antitumor potential, ferroptosis has been investigated by many groups for its potential in BC treatment. As an iron-dependent cell death process, ferroptosis is characterized by excessive oxidative phospholipids. The molecular mechanisms of ferroptosis include iron overload and the system Xc-GSH-GPX4 signaling pathway. A recent study revealed that ferroptosis is involved in the metastasis, treatment, and prognosis of BC. Herein, in this review, we comprehensively summarize the mechanism of ferroptosis, address newly identified targets involved in ferroptosis, and discuss the potential of new clinical therapies targeting ferroptosis in BC.

摘要

膀胱癌(BC)是泌尿系统癌症中最常见的类型。由于高转移率和多药耐药性,BC的预后较差。因此,迫切需要开发针对BC细胞死亡的新型疗法。作为一种具有强大抗肿瘤潜力的新型细胞死亡类型,铁死亡已被许多研究团队研究其在BC治疗中的潜力。作为一种铁依赖性细胞死亡过程,铁死亡的特征是氧化磷脂过量。铁死亡的分子机制包括铁过载和系统Xc-GSH-GPX4信号通路。最近的一项研究表明,铁死亡与BC的转移、治疗和预后有关。在此综述中,我们全面总结了铁死亡的机制,阐述了新发现的参与铁死亡的靶点,并讨论了针对BC中铁死亡的新临床疗法的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ca6/9669411/0ada3936bd2d/fphar-13-1043283-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ca6/9669411/0ada3936bd2d/fphar-13-1043283-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ca6/9669411/0ada3936bd2d/fphar-13-1043283-g001.jpg

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本文引用的文献

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Oxid Med Cell Longev. 2022 Aug 29;2022:9316847. doi: 10.1155/2022/9316847. eCollection 2022.
2
Iron oxide@chlorophyll clustered nanoparticles eliminate bladder cancer by photodynamic immunotherapy-initiated ferroptosis and immunostimulation.氧化铁@叶绿素聚集纳米颗粒通过光动力免疫治疗引发的铁死亡和免疫刺激来消除膀胱癌。
J Nanobiotechnology. 2022 Aug 11;20(1):373. doi: 10.1186/s12951-022-01575-7.
3
Pro-oxidant response and accelerated ferroptosis caused by synergetic Au(I) release in hypercarbon-centered gold(I) cluster prodrugs.
USP5通过稳定GPX4抑制膀胱癌中的铁死亡。
Curr Issues Mol Biol. 2025 Mar 20;47(3):211. doi: 10.3390/cimb47030211.
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DDR1 Targeting HOXA6 Facilitates Bladder Cancer Progression via Inhibiting Ferroptosis.靶向DDR1的HOXA6通过抑制铁死亡促进膀胱癌进展。
J Cell Mol Med. 2025 Mar;29(6):e70410. doi: 10.1111/jcmm.70410.
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Methyltransferase-like 7B participates in bladder cancer via ACSL3 mA modification in a ferroptosis manner.甲基转移酶样7B通过以铁死亡方式对ACSL3进行m⁶A修饰参与膀胱癌。
Biol Direct. 2025 Jan 20;20(1):9. doi: 10.1186/s13062-025-00597-z.
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Silencing CCT3 induces ferroptosis through the NOD1-NF-κB signaling pathway in bladder cancer.沉默 CCT3 通过 NOD1-NF-κB 信号通路诱导膀胱癌中的铁死亡。
Sci Rep. 2024 Oct 31;14(1):26188. doi: 10.1038/s41598-024-76724-z.
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