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铁死亡的分子机制及其对膀胱癌的影响。

Molecular mechanisms of ferroptosis and its effects on bladder cancer.

机构信息

First School of Clinical Medical, Gansu University of Chinese Medicince, Lanzhou 730000.

Department of Urology, 940th Hospital of Joint Logistic Support Force of Chinese People's Liberation Army, Lanzhou 730050.

出版信息

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2024 Feb 28;49(2):286-295. doi: 10.11817/j.issn.1672-7347.2024.230352.


DOI:10.11817/j.issn.1672-7347.2024.230352
PMID:38755725
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11103069/
Abstract

Bladder cancer (BC) is one of the 3 common malignant tumors in the urinary system, with high incidence, easy metastasis, poor therapeutic efficacy, and poor prognosis, which seriously threatens the health of human. Tumor cells exhibit a strong demand for iron, and iron overload can induce ferroptosis, which is an iron dependent cell death caused by lipid peroxidation and cell membrane damage. Therefore, ferroptosis has strong anti-tumor potential. The molecular mechanisms of ferroptosis is associated with abnormalities in cellular phospholipid metabolism and iron metabolism, and dysregulation of antioxidant and non-antioxidant systems Xc/glutathione (GSH)/glutathione peroxidase 4 (GPX4). Ferroptosis relevant molecules play important roles in the occurrence and development, metastasis, drug resistance, and immune response of BC, and are expected to become targets for the treatment of BC.

摘要

膀胱癌(BC)是泌尿系统 3 大常见恶性肿瘤之一,具有发病率高、易转移、疗效差、预后差等特点,严重威胁人类健康。肿瘤细胞表现出对铁的强烈需求,铁过载可诱导铁死亡,铁死亡是一种由脂质过氧化和细胞膜损伤引起的铁依赖性细胞死亡。因此,铁死亡具有很强的抗肿瘤潜力。铁死亡的分子机制与细胞磷脂代谢和铁代谢异常以及抗氧化和非抗氧化系统 Xc/谷胱甘肽 (GSH)/谷胱甘肽过氧化物酶 4 (GPX4) 的失调有关。铁死亡相关分子在 BC 的发生发展、转移、耐药和免疫反应中发挥重要作用,有望成为 BC 治疗的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5fa/11103069/84dca98cebac/ZhongNanDaXueXueBaoYiXueBan-49-2-286-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5fa/11103069/84dca98cebac/ZhongNanDaXueXueBaoYiXueBan-49-2-286-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5fa/11103069/84dca98cebac/ZhongNanDaXueXueBaoYiXueBan-49-2-286-g001.jpg

相似文献

[1]
Molecular mechanisms of ferroptosis and its effects on bladder cancer.

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2024-2-28

[2]
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[3]
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[4]
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[5]
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[6]
Evodiamine Exhibits Anti-Bladder Cancer Activity by Suppression of Glutathione Peroxidase 4 and Induction of Ferroptosis.

Int J Mol Sci. 2023-3-23

[7]
Oxidative Metabolism as a Cause of Lipid Peroxidation in the Execution of Ferroptosis.

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[8]
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Curr Neurovasc Res. 2024

[9]
Mitochondrial regulation of ferroptosis.

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[10]
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本文引用的文献

[1]
ALOX5 deficiency contributes to bladder cancer progression by mediating ferroptosis escape.

Cell Death Dis. 2023-12-7

[2]
Identification of a novel ferroptosis-inducing micropeptide in bladder cancer.

Cancer Lett. 2024-2-1

[3]
Mitochondrial-targeted brequinar liposome boosted mitochondrial-related ferroptosis for promoting checkpoint blockade immunotherapy in bladder cancer.

J Control Release. 2023-11

[4]
EP1 activation inhibits doxorubicin-cardiomyocyte ferroptosis via Nrf2.

Redox Biol. 2023-9

[5]
FLRT2 suppresses bladder cancer progression through inducing ferroptosis.

J Cell Mol Med. 2024-3

[6]
PLAGL2 promotes bladder cancer progression via RACGAP1/RhoA GTPase/YAP1 signaling.

Cell Death Dis. 2023-7-15

[7]
Advances in regulation and function of stearoyl-CoA desaturase 1 in cancer, from bench to bed.

Sci China Life Sci. 2023-12

[8]
DHODH inhibitors sensitize to ferroptosis by FSP1 inhibition.

Nature. 2023-7

[9]
FSP1: a key regulator of ferroptosis.

Trends Mol Med. 2023-9

[10]
Synergistic ferroptosis-starvation therapy for bladder cancer based on hyaluronic acid modified metal-organic frameworks.

Bioeng Transl Med. 2023-3-22

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