ArticleMolecular biotechnology2026
NRF1 Transcriptionally Regulates USP1-Mediated Deubiquitination of AURKA to Facilitate Osteosarcoma Progression.
Article in Molecular 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
backgroundThe poor prognosis of osteosarcoma (OS) lead to the low survival rate of OS patients. Numerous researches have shown that nuclear factor erythroid 2-like 1 (NRF1) can regulate the development and progression of cancer, but it has not yet been documented in OS. Therefore, the impact of NRF1 on OS progression and specific mechanisms will be investigated in this study. This may provide new ideas for the treatment of OS. The expressions of NRF1, ubiquitin-specific protease 1 (USP1), and aurora kinase A (AURKA) were determined by RT-qPCR and Western blot. CCK-8, colony formation, EdU staining, and Transwell assay were used to detect cell viability, proliferation, and invasion. Apoptosis and cell cycle were detected by flow cytometry. The deubiquitination of AURKA by USP1 was investigated by Co-IP and Western blot. The binding of NRF1 and USP1 promoter was explored by ChIP and dual-luciferase assay. A subcutaneous tumorigenic model in nude mice was used to further explore the effects of NRF1/USP1/AURKA axis on OS in vivo. NRF1, USP1, and AURKA were highly expressed in OS. The proliferation and invasion of OS cells were suppressed and apoptosis enhanced by silencing NRF1 expression. Moreover, knockdown of NRF1 inhibited tumor growth in vivo. USP1 increased AURKA stability by mediating AURKA deubiquitination. NRF1 bound to the promoter of USP1, so as to transcriptionally activate USP1 expression. USP1 overexpression reversed the effects of NRF1 knockdown on USP1 and AURKA expression and on OS cells trends and in vivo tumor growth. NRF1 transcriptionally modulated USP1, which facilitates deubiquitination of AURKA and thereby fostering OS progression.
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