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甲状腺癌中铁死亡的演变过程:新的机制和机遇。

The evolving process of ferroptosis in thyroid cancer: Novel mechanisms and opportunities.

机构信息

Thyroid Gland Breast Surgery, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, China.

Department of Hemodialysis, Huangshi Central Hospital, Huangshi, China.

出版信息

J Cell Mol Med. 2024 Aug;28(16):e18587. doi: 10.1111/jcmm.18587.

DOI:10.1111/jcmm.18587
PMID:39163517
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11335058/
Abstract

Thyroid cancer (TC) is a prevalent endocrine malignancy, with a significant increase in incidence worldwide. Ferroptosis is a novel form of programmed cell death, primarily caused by iron overload and reactive oxygen species (ROS)-dependent accumulation of lipid peroxides. The main manifestations of cellular ferroptosis are rupture of the outer membrane, crumpling of the mitochondria and shrinkage or disappearance of the mitochondrial cristae, thus leading to cell death. Ferroptosis is an important phenomenon in tumour progression, with crosstalk with tumour-associated signalling pathways profoundly affecting tumour progression, immune effects and treatment outcomes. The functions and mechanisms of ferroptosis in TC have also attracted increasing attention, mainly in terms of influencing tumour proliferation, invasion, migration, immune response, therapeutic susceptibility and genetic susceptibility. However, at present, the tumour biology of the morphological, biological and mechanism pathways of ferroptosis is much less deep in TC than in other malignancies. Hence, in this review, we highlighted the emerging role of ferroptosis in TC progression, including the novel mechanisms and potential opportunities for diagnosis and treatment, as well as discussed the limitations and prospects. Ferroptosis-based diagnostic and therapeutic strategies can potentially provide complementary management of TCs.

摘要

甲状腺癌(TC)是一种常见的内分泌恶性肿瘤,全球发病率显著增加。铁死亡是一种新的细胞程序性死亡形式,主要由铁过载和活性氧(ROS)依赖性脂质过氧化物积累引起。细胞铁死亡的主要表现为细胞膜外膜破裂、线粒体皱缩和线粒体嵴缩小或消失,从而导致细胞死亡。铁死亡是肿瘤进展中的一个重要现象,与肿瘤相关信号通路的相互作用深刻影响肿瘤的进展、免疫效应和治疗效果。铁死亡在 TC 中的功能和机制也引起了越来越多的关注,主要涉及影响肿瘤增殖、侵袭、迁移、免疫反应、治疗敏感性和遗传易感性。然而,目前,铁死亡在 TC 中的形态、生物学和机制途径的肿瘤生物学研究远不如其他恶性肿瘤深入。因此,在这篇综述中,我们强调了铁死亡在 TC 进展中的新作用,包括新的机制和诊断与治疗的潜在机会,并讨论了其局限性和前景。基于铁死亡的诊断和治疗策略可能为 TC 的管理提供补充。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4cb/11335058/6f8bb4acee45/JCMM-28-e18587-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4cb/11335058/5e709d08e53e/JCMM-28-e18587-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4cb/11335058/fff83531b370/JCMM-28-e18587-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4cb/11335058/6f8bb4acee45/JCMM-28-e18587-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4cb/11335058/5e709d08e53e/JCMM-28-e18587-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4cb/11335058/fff83531b370/JCMM-28-e18587-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4cb/11335058/6f8bb4acee45/JCMM-28-e18587-g001.jpg

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Front Oncol. 2025 Jan 23;15:1495617. doi: 10.3389/fonc.2025.1495617. eCollection 2025.

本文引用的文献

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Ferroptosis in cancer: From molecular mechanisms to therapeutic strategies.铁死亡在癌症中的作用:从分子机制到治疗策略。
Signal Transduct Target Ther. 2024 Mar 8;9(1):55. doi: 10.1038/s41392-024-01769-5.
2
Autophagy sustains mitochondrial respiration and determines resistance to BRAF inhibition in thyroid carcinoma cells.自噬维持线粒体呼吸,并决定甲状腺癌细胞对 BRAF 抑制的耐药性。
Autophagy. 2024 Jun;20(6):1383-1397. doi: 10.1080/15548627.2024.2312790. Epub 2024 Mar 4.
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Thyroid Cancer: A Review.甲状腺癌:综述。
JAMA. 2024 Feb 6;331(5):425-435. doi: 10.1001/jama.2023.26348.
4
Elucidating the role of Pyroptosis in papillary thyroid cancer: prognostic, immunological, and therapeutic perspectives.阐明细胞焦亡在甲状腺乳头状癌中的作用:预后、免疫学及治疗方面的观点
Cancer Cell Int. 2024 Jan 29;24(1):45. doi: 10.1186/s12935-024-03229-0.
5
Genomic alterations in thyroid cancer: biological and clinical insights.甲状腺癌的基因组改变:生物学和临床见解。
Nat Rev Endocrinol. 2024 Feb;20(2):93-110. doi: 10.1038/s41574-023-00920-6. Epub 2023 Dec 4.
6
Anaplastic thyroid cancer cells reduce CD71 levels to increase iron overload tolerance.间变性甲状腺癌细胞降低 CD71 水平以增加铁过载耐受性。
J Transl Med. 2023 Nov 3;21(1):780. doi: 10.1186/s12967-023-04664-9.
7
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Environ Toxicol. 2024 Mar;39(3):1129-1139. doi: 10.1002/tox.23992. Epub 2023 Oct 20.
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