ArticleCancer research2025
Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity.
Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Profiling of Yeast Saccharomyces cerevisiae Mitochondrial AMPylome Reveals a Regulation of OXPHOS Coupling through ATP Synthase Subunit Delta.Journal of proteome research · 2026Article
- Yeast β-glucan selenium nanoparticles enhance meat quality in heat-stressed broilers via SelO-mediated mitochondrial biogenesis and oxidative myofiber remodeling.Journal of animal science and biotechnology · 2026Article
- Selenoproteins: Minute yet vital players governing cellular fate.Genes & diseases · 2026Review
- DHX37 and tumor growth: a novel avenue for melanoma research.Journal of translational medicine · 2026Article
- Genetics of selenoproteins and selenoprotein metabolism - An overview of current concepts and emerging aspects.Redox biology · 2026Review
- Tracing the vertebrate selenoproteome evolution reveals expansions in ray-finned fishes and convergent depletions in tetrapods.BMC genomics · 2026Article
- Radiation-induced autophagy regulates fibroblast mitochondrial metabolism and crosstalk with triple-negative breast cancer cells.Cell reports · 2026Article
- GPR44-Dependent Regulation of the Selenoproteome by eIF4a3 in Murine Acute Myeloid Leukemia-Initiating Stem Cells.Biological trace element research · 2026Article
- Impaired redox adaptation through SLC38A5-dependent glutamine metabolism contributes to melatonin-mediated anoikis sensitivity and metastasis suppression in bone cancer.International journal of biological sciences · 2026Article
- Metabolic Functions and Mechanisms of Selenium, Selenocysteine, and GPX4 Mediated Immune Regulation Through Autophagy in Solid Tumors.Food science & nutrition · 2025Review
- Ribonuclease RNase Z is an evolutionarily conserved deAMPylase.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The rise of AMPylation: from bacterial beginnings to modern implications in health and disease.Biochemical Society transactions · 2025Review
- A repurposed AMP binding domain reveals mitochondrial protein AMPylation as a regulator of cellular metabolism.Nature communications · 2025Article
- Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025Review
- Metabolic reprogramming in melanoma therapy.Cell death discovery · 2025Review
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Authors and funding
18 authors.
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Abstract
Evolutionarily conserved selenoprotein O (SELENOO) catalyzes a posttranslational protein modification known as AMPylation that is essential for the oxidative stress response in bacteria and yeast. Given that oxidative stress experienced in the blood limits survival of metastasizing melanoma cells, SELENOO might be able to affect metastatic potential. However, further work is needed to elucidate the substrates and functional relevance of the mammalian homolog of SELENOO. In this study, we revealed that SELENOO promotes cancer metastasis and identified substrates of SELENOO in mammalian mitochondria. In patients with melanoma, high SELENOO expression was correlated with metastasis and poor overall survival. In a murine model of spontaneous melanoma metastasis, SELENOO deficiency significantly reduced metastasis to distant visceral organs, which could be rescued by treatment with the antioxidant N-acetylcysteine. Mechanistically, SELENOO AMPylated multiple mitochondrial substrates, including succinate dehydrogenase subunit A, one of the four key subunits of mitochondrial complex II. Consistently, SELENOO-deficient cells featured increased mitochondrial complex II activity. Together, these findings demonstrate that SELENOO deficiency limits melanoma metastasis by modulating mitochondrial function and oxidative stress. Significance: SELENOO alters mitochondrial function and supports metastasis in melanoma, highlighting the impact of SELENOO-mediated posttranslational modification of mitochondrial substrates and selenoproteins in cancer progression.
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