ArticleApplied biochemistry and biotechnology2026
UCHL3 Promotes Triple-Negative Breast Cancer Metastatic Potential Through Enhancing Cell Migration and Invasion.
Article in Applied biochemistry and biotechnology, 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
Ubiquitin carboxyl-terminal hydrolase L3 (UCHL3), a key deubiquitinating enzyme of the UCH family, has been implicated in DNA repair in breast cancer; however, its role in regulating cell migration and invasion in triple-negative breast cancer (TNBC) remains poorly understood. The expression pattern of UCHL3 across breast cancer subtypes was analyzed using TCGA data. In TNBC cells, UCHL3 mRNA levels were quantified by qRT-PCR, while its protein expression and epithelial-mesenchymal transition (EMT) markers (Vimentin, N-cadherin, SNAIL, E-cadherin, α-SMA, TWIST) were assessed by Western blot. Functional assays included: MTT and EdU incorporation assays for proliferation; wound healing and Transwell migration assays for migratory capacity. Transcriptomic changes induced by UCHL3 knockdown were profiled via RNA sequencing. Additionally, an in vivo mice model was used to evaluate the pro-invasive effects of UCHL3 overexpression in TNBC. UCHL3 was significantly overexpressed in TNBC and correlated with poor patient prognosis. Functional studies revealed that UCHL3 enhances the proliferative capacity of TNBC cells. Furthermore, UCHL3 was demonstrated to promote TNBC cell migration and invasion through modulation of epithelial-mesenchymal transition (EMT) markers. Mechanistically, knockdown of UCHL3 attenuated activation of invasion- and migration-related signaling pathways in TNBC cells. Pharmacological inhibition of UCHL3 effectively suppressed TNBC cell migration and invasion in vitro. In vivo studies further confirmed that UCHL3 overexpression drives metastatic progression of TNBC in mice. UCHL3 is significantly upregulated in TNBC and drives tumor progression by promoting cell proliferation and activating EMT-mediated migration and invasion. These findings identify UCHL3 as a potential therapeutic target for TNBC treatment.
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