ArticleEpigenetics2026
Aurora kinase a phosphorylates and stabilizes UHRF1 to maintain DNA methylation and prostate cancer cell survival.
Article in Epigenetics, 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
Aberrant DNA methylation is a hallmark of prostate cancer (PCa) and plays a critical role in sustaining the epigenetic silencing of tumor suppressor genes. However, how oncogenic signaling pathways interface with the DNA methylation machinery remains poorly understood. In this study, we identify AURKA as a key regulator of global DNA methylation in PCa cells. AURKA depletion markedly reduces genomic 5-methylcytosine (5mC) levels, indicating its essential role in DNA methylation maintenance. Mechanistically, AURKA directly interacts with UHRF1-a crucial epigenetic regulator that recruits DNMT1 to hemimethylated DNA, and phosphorylates it at Ser76, thereby enhancing UHRF1 protein stability. AURKA depletion accelerates UHRF1 degradation via the ubiquitin-proteasome pathway, whereas AURKA overexpression stabilizes UHRF1 by suppressing its polyubiquitination. The phospho-deficient UHRF1 S76A mutant exhibits reduced stability and increased polyubiquitination, confirming that phosphorylation at Ser76 is critical for AURKA-mediated UHRF1 stabilization. Functionally, disruption of the AURKA-UHRF1 axis de-represses
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