ArticleCell death & disease2024
Maintenance of magnesium homeostasis by NUF2 promotes protein synthesis and anaplastic thyroid cancer progression.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- NUF2 interacts with BUB3 and drives lung adenocarcinoma progression through activation of the NF-κB pathway.World journal of surgical oncology · 2026Article
- Causal relationship between metabolic syndrome and gastric cancer: insights from comprehensive analysis and biomarker identification.Translational cancer research · 2026Article
- Uncovering novel functions of NUF2 in glioblastoma and MRI-based expression prediction.Scientific reports · 2025Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
Thyroid cancer is the most frequently observed endocrine-related malignancy among which anaplastic thyroid cancer (ATC) is the most fatal subtype. The synthesis of protein is active to satisfy the rapid growth of ATC tumor, but the mechanisms regulating protein synthesis are still unknown. Our research revealed that kinetochore protein NUF2 played an essential role in protein synthesis and drove the progression of ATC. The prognosis of patients with thyroid carcinoma was positively correlated with high NUF2 expression. Depletion of NUF2 in ATC cells notably inhibited the proliferation and induced apoptosis, while overexpression of NUF2 facilitated ATC cell viability and colony formation. Deletion of NUF2 significantly suppressed the growth and metastasis of ATC in vivo. Notably, knockdown of NUF2 epigenetically inhibited the expression of magnesium transporters through reducing the abundance of H3K4me3 at promoters, thereby reduced intracellular Mg
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