ArticleMolecular oncology2023
NUAK1 governs centrosome replication in pancreatic cancer via MYPT1/PP1β and GSK3β-dependent regulation of PLK4.
Article in Molecular oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Chemical Genetic Screen Identifies PSD3 as a Direct Substrate of NUAK1 that Regulates Dendritic Spine Maturation.bioRxiv : the preprint server for biology · 2026Article
- HNRNPF Increases MAF and CCNB2 Levels To Promote Cancer Cell Stemness and Progression of Pancreatic Ductal Adenocarcinoma.Stem cell reviews and reports · 2026Article
- NUAK1 silencing enhances radiotherapy-induced ferroptosis in locally advanced rectal cancer by impairing Nrf2-driven transcription of GPX4.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Insights into targeting LKB1 in tumorigenesis.Genes & diseases · 2025Review
- The role of AMPK in pancreatic cancer: from carcinogenesis to treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- NUAK: never underestimate a kinase.Essays in biochemistry · 2024Review
- Novel kinase 1 regulates CD8+T cells as a potential therapeutic mechanism for idiopathic pulmonary fibrosis.International journal of medical sciences · 2024Article
- Kinase signalling adaptation supports dysfunctional mitochondria in disease.Frontiers in molecular biosciences · 2024Review
- NUAK1 promotes tumor metastasis through upregulating slug transcription in esophageal squamous cell carcinoma.Cancer cell international · 2023Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
The AMP-activated protein kinase (AMPK)-related kinase NUAK1 (NUAK family SNF1-like kinase 1) has emerged as a potential vulnerability in MYC-dependent cancer but the biological roles of NUAK1 in different settings are poorly characterised, and the spectrum of cancer types that exhibit a requirement for NUAK1 is unknown. Unlike canonical oncogenes, NUAK1 is rarely mutated in cancer and appears to function as an obligate facilitator rather than a cancer driver per se. Although numerous groups have developed small-molecule NUAK inhibitors, the circumstances that would trigger their use and the unwanted toxicities that may arise as a consequence of on-target activity are thus undetermined. Reasoning that MYC is a key effector of RAS pathway signalling and the GTPase KRAS is almost uniformly mutated in pancreatic ductal adenocarcinoma (PDAC), we investigated whether this cancer type exhibits a functional requirement for NUAK1. Here, we show that high NUAK1 expression is associated with reduced overall survival in PDAC and that inhibition or depletion of NUAK1 suppresses growth of PDAC cells in culture. We identify a previously unknown role for NUAK1 in regulating accurate centrosome duplication and show that loss of NUAK1 triggers genomic instability. The latter activity is conserved in primary fibroblasts, raising the possibility of undesirable genotoxic effects of NUAK1 inhibition.
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