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甲状腺癌中的泛素修饰酶:机制与功能

Ubiquitin-modifying enzymes in thyroid cancer:Mechanisms and functions.

作者信息

Xiong Xingmin, Huang BenBen, Gan Zhe, Liu Weixiang, Xie Yang, Zhong Jianing, Zeng Xiangtai

机构信息

Department of Thyroid and Hernia Surgery, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, 341000, China.

Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, Gannan Medical University, 323 National Road, Ganzhou, 341000, Jiangxi, China.

出版信息

Heliyon. 2024 Jul 2;10(13):e34032. doi: 10.1016/j.heliyon.2024.e34032. eCollection 2024 Jul 15.

DOI:10.1016/j.heliyon.2024.e34032
PMID:39091932
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11292542/
Abstract

Thyroid cancer is the most common malignant tumor of the endocrine system, and evidence suggests that post-translational modifications (PTMs) and epigenetic alterations play an important role in its development. Recently, there has been increasing evidence linking dysregulation of ubiquitinating enzymes and deubiquitinases with thyroid cancer. This review aims to summarize our current understanding of the role of ubiquitination-modifying enzymes in thyroid cancer, including their regulation of oncogenic pathways and oncogenic proteins. The role of ubiquitination-modifying enzymes in thyroid cancer development and progression requires further study, which will provide new insights into thyroid cancer prevention, treatment and the development of novel agents.

摘要

甲状腺癌是内分泌系统最常见的恶性肿瘤,证据表明翻译后修饰(PTMs)和表观遗传改变在其发展过程中起重要作用。最近,越来越多的证据表明泛素化酶和去泛素化酶的失调与甲状腺癌有关。本综述旨在总结我们目前对泛素化修饰酶在甲状腺癌中的作用的理解,包括它们对致癌途径和致癌蛋白的调控。泛素化修饰酶在甲状腺癌发生和发展中的作用需要进一步研究,这将为甲状腺癌的预防、治疗和新型药物的开发提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4163/11292542/cb591e029e64/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4163/11292542/24e2af3110dc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4163/11292542/3fb6777da77e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4163/11292542/cb591e029e64/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4163/11292542/24e2af3110dc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4163/11292542/3fb6777da77e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4163/11292542/cb591e029e64/gr3.jpg

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本文引用的文献

1
GSG2 promotes thyroid cancer via stabilizing AURKB and activating AKT pathway.GSG2 通过稳定 AURKB 和激活 AKT 通路促进甲状腺癌。
Aging (Albany NY). 2024 Mar 4;16(6):5091-5107. doi: 10.18632/aging.205605.
2
Cytosolic Cadherin 4 promotes angiogenesis and metastasis in papillary thyroid cancer by suppressing the ubiquitination/degradation of β-catenin.细胞质钙黏蛋白 4 通过抑制β-连环蛋白的泛素化/降解促进甲状腺乳头状癌的血管生成和转移。
J Transl Med. 2024 Feb 24;22(1):201. doi: 10.1186/s12967-024-05012-1.
3
RNF115 aggravates tumor progression through regulation of CDK10 degradation in thyroid carcinoma.
RNF115通过调控甲状腺癌中CDK10的降解来促进肿瘤进展。
Cell Biol Toxicol. 2024 Feb 20;40(1):14. doi: 10.1007/s10565-024-09845-w.
4
Ubiquitin-specific peptidase 10 attenuates the ferroptosis to promote thyroid cancer malignancy by facilitating GPX4 via elevating SIRT6.泛素特异性肽酶 10 通过上调 SIRT6 促进 GPX4 从而减弱铁死亡以促进甲状腺癌恶性转化。
Environ Toxicol. 2024 Mar;39(3):1129-1139. doi: 10.1002/tox.23992. Epub 2023 Oct 20.
5
Upregulation of ubiquitin carboxy‑terminal hydrolase 47 (USP47) in papillary thyroid carcinoma ex vivo and reduction of tumor cell malignant behaviors after USP47 knockdown by stabilizing SATB1 expression in vitro.甲状腺乳头状癌中泛素羧基末端水解酶47(USP47)的体外上调以及通过体外稳定SATB1表达在USP47敲低后肿瘤细胞恶性行为的降低。
Oncol Lett. 2023 Jul 17;26(3):370. doi: 10.3892/ol.2023.13956. eCollection 2023 Sep.
6
ISG15 and ISGylation modulates cancer stem cell-like characteristics in promoting tumor growth of anaplastic thyroid carcinoma.ISG15 和 ISGylation 调节癌症干细胞样特征,促进间变性甲状腺癌的肿瘤生长。
J Exp Clin Cancer Res. 2023 Jul 27;42(1):182. doi: 10.1186/s13046-023-02751-9.
7
Expression and regulatory network of E3 ubiquitin ligase NEDD4 family in cancers.E3 泛素连接酶 NEDD4 家族在癌症中的表达与调控网络。
BMC Cancer. 2023 Jun 8;23(1):526. doi: 10.1186/s12885-023-11007-w.
8
Paradoxes of Cellular SUMOylation Regulation: A Role of Biomolecular Condensates?细胞 SUMOylation 调控的悖论:生物分子凝聚物的作用?
Pharmacol Rev. 2023 Sep;75(5):979-1006. doi: 10.1124/pharmrev.122.000784. Epub 2023 May 3.
9
RNF150 suppresses papillary thyroid carcinoma with ASK1 ubiquitination presenting a direct target via inactivating p38 signaling axis.RNF150 通过抑制 ASK1 泛素化来抑制甲状腺乳头状癌,从而通过失活 p38 信号轴来呈现直接靶标。
Cell Biol Int. 2023 Jul;47(7):1198-1208. doi: 10.1002/cbin.12011. Epub 2023 Mar 23.
10
The roles of E3 ubiquitin ligases in cancer progression and targeted therapy.E3 泛素连接酶在癌症进展和靶向治疗中的作用。
Clin Transl Med. 2023 Mar;13(3):e1204. doi: 10.1002/ctm2.1204.