ArticleActa pharmaceutica Sinica. B2025
CDK1-mediated phosphorylation of USP37 regulates SND1 stability and promotes oncogenesis in colorectal cancer.
Article in Acta pharmaceutica Sinica. B, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Computational Investigation of S781F Mutation-Induced Remodeling of the Staphylococcal Nuclease Domain-Containing Protein 1-Argonaute 2 Interface.International journal of molecular sciences · 2026Article
- Investigating the mechanisms of malignant progression in colorectal cancer using weighted gene co-expression network analysis and machine learning.Journal of molecular histology · 2026Article
- CHK2-USP37 axis stabilizes FOXO4 to sustain senescence and evade apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- An integrative pan-cancer analysis of USP37 and functional validation in pancreatic cancer.Frontiers in cell and developmental biology · 2025Article
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Authors and funding
10 authors.
Funding
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Abstract
Colorectal cancer (CRC) poses a severe global health challenge with high incidence and mortality rates. USP37 has been identified as the bona fide deubiquitinase of SND1, playing a critical role in stabilizing SND1, thereby augmenting its oncogenic potential. The interaction between USP37 and SND1 was confirmed through extensive proteomics, ubiquitinomics, and interactomics, underscoring their synergistic effects on CRC proliferation and metastasis. Additionally, CDK1 has emerged as a pivotal regulator of USP37, phosphorylating it at threonine 631 rather than serine 628, enhancing its deubiquitinase activity, and consequently stabilizing SND1 to drive CRC malignancy further. Histological analyses of human CRC samples linked the upregulation of CDK1 and USP37 with increased SND1 levels and poor patient prognosis. High-throughput virtual screening and subsequent experimental validation identified Dacarbazine as a pharmacological inhibitor of USP37, and its inhibition disrupted SND1 stability, hindering CRC cell proliferation and metastasis. This study reveals a novel and promising molecular mechanism driving CRC progression through the CDK1-USP37-SND1 axis, highlighting the clinical importance of targeting this pathway to improve patient outcomes.
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