ArticleNature structural & molecular biology2025
ERK-USP9X-coupled regulation of thymidine kinase 1 promotes both its enzyme activity-dependent and its enzyme activity-independent functions for tumor growth.
Article in Nature structural & molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Elevated thymidine kinase 1 expression at baseline predicts poor prognosis in breast cancer patients.Frontiers in oncology · 2026Pooled it
- Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer.Signal transduction and targeted therapy · 2026Review
- KIF26B promotes bladder cancer progression through activating the NF-κB signaling pathway.iScience · 2026Article
- Genetic variation and proliferation-promoting virulence function of thymidine kinase from Paulownia witches' broom phytoplasma.BMC plant biology · 2026Article
- Integrating machine learning and single-cell sequencing to reveal the role of kinase-related genes in subtype classification and prognostic significance of lung squamous cell carcinoma.Discover oncology · 2026Article
- Vitamin D attenuates the progression of pulmonary fibrosis via inhibiting thymidine kinase 1/PFKFB3-driven glycolysis.Journal of translational medicine · 2026Article
- Histone lactylation-driven feedback loop modulates pyrimidine metabolism to promote oral carcinogenesis.Cell death & disease · 2026Article
- TK1 in gastric cancer: Helicobacter pylori-driven oncogenesis biomarker, utility, and emerging targeted therapies.Frontiers in oncology · 2026Review
- Quercetin inhibits gastric cancer cell proliferation and migration and is associated with the suppression of the IDO1-Kynurenine-AhR axis.BMC cancer · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thymidine kinase 1 (TK1), a crucial enzyme in DNA synthesis, is highly expressed in various cancers. However, the mechanisms underlying its elevated expression and the implications for tumor metabolism remain unclear. Here we demonstrate that activation of growth factor receptors enhances TK1 expression. Treatment with epidermal growth factor or insulin-like growth factor 1 induces the binding of ERK1/2 to TK1 and subsequent TK1 S13/231 phosphorylation by ERK1/2. This modification recruits ubiquitin carboxyl-terminal hydrolase 9X to deubiquitylate TK1, preventing its proteasomal degradation. Stabilized TK1 not only enhances its enzyme activity-dependent deoxythymidine monophosphate production for DNA synthesis but also promotes glycolysis independently of its enzymatic activity by upregulating phosphofructokinase/fructose bisphosphatase type 3 expression. This dual role of TK1 drives the proliferation of human hepatocellular carcinoma cells and liver tumor growth in mice. Our findings reveal a crucial mechanism by which growth factors promote tumor development through TK1-mediated DNA synthesis and glycolysis and highlight TK1 as a potential molecular target for cancer treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.