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Updated: Sep 27, 2025

Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
USP26 promotes anaplastic thyroid cancer progression by stabilizing TAZ
Jianing Tang1, Yongwen Luo2, Liang Xiao3
1Department of Liver Surgery, Xiangya Hospital, Clinical Research Center for Breast Cancer Control and Prevention in Hunan Province, Central South University, Changsha, China. tjn1995@whu.edu.cn.
Researchers found that USP26 deubiquitylase stabilizes TAZ protein in anaplastic thyroid cancer (ATC). Inhibiting USP26 reduced cancer cell growth and invasion, suggesting USP26 as a potential therapeutic target for aggressive ATC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Anaplastic thyroid cancer (ATC) is an aggressive malignancy with limited treatment options.
- The Hippo pathway, regulated by key effectors like TAZ, is crucial in carcinogenesis.
- Mechanisms driving abnormal TAZ expression in ATC are not fully understood.
Purpose of the Study:
- To identify factors responsible for TAZ stabilization in ATC.
- To investigate the role of USP26 as a deubiquitylase for TAZ in ATC.
- To explore USP26 as a potential therapeutic target for ATC.
Main Methods:
- Identified USP26 as a deubiquitylase interacting with and stabilizing TAZ in ATC cells.
- Assessed the impact of USP26 depletion on ATC cell proliferation, migration, and invasion.
- Analyzed TAZ protein levels and expression of TAZ/TEAD target genes (CTGF, ANKRD1, CYR61) following USP26 depletion.
Main Results:
- USP26 directly deubiquitylates and stabilizes TAZ in anaplastic thyroid cancer.
- USP26 depletion significantly inhibited ATC cell proliferation, migration, and invasion.
- USP26 depletion reduced TAZ protein levels and suppressed TAZ/TEAD target gene expression.
Conclusions:
- USP26 functions as a deubiquitylating enzyme for TAZ in ATC.
- USP26 stabilizes TAZ, promoting aggressive phenotypes in anaplastic thyroid cancer.
- Targeting USP26 may offer a novel therapeutic strategy for ATC.
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