ArticleJournal of molecular histology2026
The deubiquitinating enzyme USP42 promotes lung adenocarcinoma progression through PTGS2.
Article in Journal of molecular histology, 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
The ubiquitin-specific peptidase 42 (USP42) is a cysteine-dependent deubiquitinase with pro-tumorigenic roles in several cancers. In lung adenocarcinoma (LUAD), elevated USP42 expression correlates with advanced stage and poor survival, mirroring the prognostic impact of prostaglandin-endoperoxide synthase 2 (PTGS2) overexpression. However, the substrate repertoire and mechanisms by which USP42 drives malignant progression and immune evasion in LUAD remain largely undefined. Using TCGA datasets and functional experiments in LUAD cell lines, we found that USP42 is significantly overexpressed in LUAD, and its high expression is associates with advanced stages and reduced overall survival. Besides, USP42 knockdown suppressed proliferation, colony formation, migration, invasion, and epithelial-mesenchymal transition (EMT). Mechanistically, USP42 physically interacted with PTGS2, thereby stabilizing PTGS2 from proteasomal degradation. Mouse Lewis lung carcinoma (LLC) cells with USP42 knockdown were subcutaneously injected into C57BL/6 mice. Our results demonstrated that USP42 depletion attenuated tumor growth, reduced PTGS2 and PD-L1 expression, alleviated CD8
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