ArticleJournal of translational medicine2026
UBE2M promotes malignant phenotypes of prostate cancer through mediating NAA10 neddylation.
Article in Journal of translational medicine, 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
backgroundProstate cancer (PCa) is a common malignant tumor in men, with a high incidence rate, posing a serious threat to human health and quality of life. Neddylation is a major post-translation modification, which is essential for multiple cellular behaviors. Aberrant neddylation has been implicated in the development and progression of various diseases. The NEDD8-conjugating enzyme UBE2M is frequently overexpressed in multiple types of malignancies and is closely associated with tumor initiation, progression, metastasis, and therapy resistance. However, the potential role of UBE2M in prostate cancer remains unknown.
methodsIn our study, a bioinformatics analysis and Immunohistochemistry were employed to validate elevated UBE2M expression in prostate cancer compared to adjacent tissues. We assessed the impact of UBE2M on tumor progression using in vitro and in vivo functional experiments, including CCK8, colony formation, transwell assay and several animal models including PCa xenografts were employed to investigate the role of UBE2M in PCa progression. To elucidate the mechanism, we utilized Coimmunoprecipitation, Mass spectrometry analysis and Proximity ligation assay to elucidate the mechanisms by which UBE2M functions in prostate cancer cells.
resultsWe discovered that UBE2M expression is significantly elevated in prostate cancer tissues compared to adjacent paracancerous tissues, and this high UBE2M expression indicates a poorer prognosis for patients. Functional experiments demonstrated that overexpression of UBE2M promotes the proliferation and migration of prostate cancer cells, whereas knockdown of UBE2M inhibits these malignant phenotypes. Furthermore, we identified that NAA10 undergoes neddylation modification, and elucidated that the RBX1-CUL4A complex acts as the critical E3 ligase responsible for this modification, with the K148 site being the key neddylation site. We further confirmed that UBE2M enhances the protein stability and functional activity of NAA10 by promoting its neddylation. Knockdown of NAA10 significantly suppressed the UBE2M-driven proliferation of prostate cancer cells.
conclusionsThis study reveals that UBE2M drives prostate cancer tumorigenesis by facilitating NAA10 neddylation.
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