2. Academic Validation
  3. GPR34 Stabilized by Deubiquitinase USP8 Suppresses Ferroptosis of ATC

GPR34 Stabilized by Deubiquitinase USP8 Suppresses Ferroptosis of ATC

  • Mediators Inflamm. 2025 Aug 18:2025:5576056. doi: 10.1155/mi/5576056.
Bokang Yan 1 2 3,  Jiaxing Guo 4,  Meiyuan Huang 3,  Zhecheng Li 5,  Jingyue Sun 6,  Hailong Tan 5,  Weiwei Lai 7,  Shi Chang 2 5 8
Affiliations

Affiliations

  • 1 Institute of Large-Scale Scientific Facility and Centre for Zero Magnetic Field Science, Beihang University, Beijing 100191, China.
  • 2 National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, Hunan, China.
  • 3 Department of Pathology, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou 412007, Hunan, China.
  • 4 Department of Hematology, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou 412007, Hunan, China.
  • 5 Department of General Surgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan, China.
  • 6 Department of Pathology, Xiangya Hospital, Central South University, Changsha 410078, Hunan, China.
  • 7 Hunan Provincial Key Laboratory of Pediatric Orthopedics, The Affiliated Children's Hospital of Xiangya School of Medicine, Central South University, Changsha 410007, Hunan, China.
  • 8 Clinical Research Center for Thyroid Disease in Hunan Province, Changsha 410008, Hunan, China.
PMID: 40862294 DOI: 10.1155/mi/5576056
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.

Keywords

ATC; DUB-IN-3; GPR34; USP8; ferroptosis.

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