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去泛素化酶USP8稳定的GPR34抑制甲状腺未分化癌的铁死亡

GPR34 Stabilized by Deubiquitinase USP8 Suppresses Ferroptosis of ATC.

作者信息

Yan Bokang, Guo Jiaxing, Huang Meiyuan, Li Zhecheng, Sun Jingyue, Tan Hailong, Lai Weiwei, Chang Shi

机构信息

Institute of Large-Scale Scientific Facility and Centre for Zero Magnetic Field Science, Beihang University, Beijing 100191, China.

National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, Hunan, China.

出版信息

Mediators Inflamm. 2025 Aug 18;2025:5576056. doi: 10.1155/mi/5576056. eCollection 2025.

Abstract

G protein-coupled receptor 34 (GPR34) is an orphan receptor within the G protein-coupled receptor (GPCR) superfamily, and its specific role in anaplastic thyroid carcinoma (ATC) remains to be elucidated. In this study, we observed that GPR34 was aberrantly upregulated in ATC and the deletion of GPR34 inhibited tumor progression both in vivo and in vitro. Additionally, suppression of GPR34 promoted ferroptosis in ATC cells. We further identified USP8 as a deubiquitinase (DUB) for GPR34, and the effects induced by GPR34 deletion were reversible through USP8 overexpression. Moreover, targeting USP8 with the inhibitor DUB-IN-3 effectively restrained ATC growth. Together, the present study revealed the role of GPR34 in ATC progression and ferroptosis, discovered its corresponding DUBs, and proposed GPR34 as a promising target for ATC therapy.

摘要

G蛋白偶联受体34(GPR34)是G蛋白偶联受体(GPCR)超家族中的一种孤儿受体,其在间变性甲状腺癌(ATC)中的具体作用仍有待阐明。在本研究中,我们观察到GPR34在ATC中异常上调,GPR34的缺失在体内和体外均抑制肿瘤进展。此外,GPR34的抑制促进了ATC细胞中的铁死亡。我们进一步鉴定出USP8是GPR34的去泛素化酶(DUB),通过USP8过表达,GPR34缺失诱导的效应是可逆的。此外,用抑制剂DUB-IN-3靶向USP8可有效抑制ATC生长。总之,本研究揭示了GPR34在ATC进展和铁死亡中的作用,发现了其相应的DUB,并提出GPR34作为ATC治疗的一个有前景的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca63/12377955/e0ed82862ea6/MI2025-5576056.001.jpg

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