ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Tip60-Mediated USP22 Lactylation Drives Glutamine Metabolic Reprogramming via SLC25A5 in TNBC.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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
Glutamine metabolism promotes breast cancer progression and metastasis, though the underlying mechanisms are not fully understood. In this study, we identified a significant positive correlation between glutamine metabolism and ubiquitin-specific protease 22 (USP22)expression in breast cancer patients. USP22 drives glutamine reprogramming to promote lactate secretion, thereby supporting triple-negative breast cancer (TNBC) growth and survival. This process involves the lactyltransferase Tat-interactive protein, 60 kDa (Tip60), which catalyzes K134 lactylation of USP22. This post-translational modification (PTM) stabilizes USP22 protein levels and facilitates its mitochondrial location. Moreover, USP22 stabilizes the solute carrier family 25 member 5 (SLC25A5) through its de-ubiquitinase activity. Clinically, increased expression levels of both USP22 and SLC25A5 are significantly associated with a poor prognosis in patients with TNBC. Furthermore, USP22 regulates glutamine metabolism to promote α-ketoglutarate (α-KG) secretion, thereby activating M2 macrophages and suppressing the anti-tumor immune response. Importantly, targeting USP22 synergized with CB-839 in TNBC xenograft models. These findings underscore USP22 as a promising therapeutic target for TNBC.
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