ArticleCancer biology & therapy2026
UCHL5 suppresses thyroid carcinoma progression via ZRANB1 stabilization and ferroptosis regulation.
Article in Cancer biology & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThis study investigated the role of UCHL5 in thyroid carcinoma (THCA) progression, focusing on its tumor-suppressive mechanisms and regulation of ferroptosis.
methodsWe performed multi-omics analysis of TCGA and GEO datasets and validated the findings using clinical samples. The CRISPR/Cas9-mediated knockout and stable overexpression in THCA cell lines were constructed, followed by comprehensive functional assays including co-immunoprecipitation (Co-IP), ubiquitination analysis, xenograft tumor models, and ferroptosis sensitivity tests using erastin/ferrostatin-1 with BODIPY C11 lipid ROS measurement. Weighted gene co-expression network analysis (WGCNA) was performed to identify hub genes and to analyze associated pathways.
resultsClinical data revealed significant downregulation of UCHL5 in advanced thyroid cancers, particularly in lymph node metastases. UCHL5 knockout markedly accelerated cell proliferation and xenograft tumor growth, while its overexpression suppressed both. Mechanistically, we identified a direct interaction between UCHL5 and ZRANB1 through co-IP, with UCHL5 extending the protein half-life of ZRANB1 by over 2-fold. In ferroptosis regulation, erastin treatment (10 μM) revealed that UCHL5 overexpression enhanced sensitivity, while UCHL5 knockout conferred significant protection, accompanied by altered GSH levels, Fe²⁺ accumulation, and lipid ROS production. Western blot analysis revealed that UCHL5 upregulated ZRANB1 and downregulated SLC7A11/GPX4 expression.
conclusionThis study demonstrates that UCHL5 acts as a critical tumor suppressor in thyroid cancer by stabilizing ZRANB1 through deubiquitination and regulating ferroptosis via the SLC7A11-GPX4 axis.
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