ArticleDiscover oncology2026
UCHL1 promotes osteosarcoma progression via deubiquitination and stabilization of LDHB.
Article in Discover oncology, 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
Osteosarcoma is an aggressive bone malignancy with limited treatment options. Ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) is implicated in tumor progression, but its role in osteosarcoma remains unclear. This study investigates UCHL1's function and explores cryptochlorogenic acid (CCA) as a potential inhibitor. Bioinformatics analysis of GEO datasets (GSE19276, GSE152048) identified UCHL1 overexpression in osteosarcoma. In vitro experiments used Saos2 cells for UCHL1 knockdown (shRNA) and CCA treatment, assessing proliferation (CCK-8, EdU), migration (Transwell, wound healing), and apoptosis (Western blot). Co-immunoprecipitation and ubiquitination assays evaluated UCHL1-LDHB interaction. In vivo, subcutaneous xenograft models tested CCA and UCHL1-LDHB efficacy in mice. UCHL1 was overexpressed in osteosarcoma tissues and Saos2 cells. UCHL1 knockdown suppressed proliferation, migration, and upregulated apoptosis markers (Bax, caspase-8/9). Mechanistically, UCHL1 bound and deubiquitinated LDHB, stabilizing this metabolic enzyme. LDHB knockdown reversed UCHL1-driven oncogenesis. Virtual screening identified CCA as a UCHL1 inhibitor, forming hydrogen bonds with Cys90/Phe160. CCA treatment inhibited Saos2 proliferation, migration, and tumor growth in vivo. Xenografts showed reduced PCNA and elevated Bax expression with CCA. UCHL1 promotes osteosarcoma progression by stabilizing LDHB via deubiquitination. CCA, a natural UCHL1 inhibitor, demonstrates significant anti-tumor efficacy, offering a novel therapeutic strategy for osteosarcoma.
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