ArticleCell & bioscience2023
Post-translational modification of CDK1-STAT3 signaling by fisetin suppresses pancreatic cancer stem cell properties.
Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- The KAT8-CDK1 K33 acetylation axis drives doxorubicin resistance by suppressing ferroptosis and apoptosis in breast cancer.Cell death & disease · 2026Article
- Decoding the Post-translational Modification Crosstalk: Functional Implications of Phosphorylation, Acetylation, and Methylation.The journal of physical chemistry. B · 2026Article
- Acetylation modification in malignant progression and therapeutic resistance of gliomas.Frontiers in cell and developmental biology · 2026Review
- An Overview of Targeting Some Cancer Hallmarks with Plant Polyphenols: A Step Toward Precision.Sub-cellular biochemistry · 2026Review
- Post-Translational Modifications: Key "Regulators" of Pancreatic Cancer Malignant Phenotype-Advances in Mechanisms and Targeted Therapies.Biomedicines · 2025Review
- STAT3 axis in cancer and cancer stem cells: From oncogenesis to targeted therapies.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- CDK1 drives SOX9-mediated chemotherapeutic resistance in gastric cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Kaempferol triggers cellular senescence via CDK1 ubiquitination in HCC cells.Cancer cell international · 2025Article
- Review
- Phosphorylation of USP33 by CDK1 stabilizes the mTORC2 component SIN1.Cell death & disease · 2025Article
- Natural Killer Cell Activation Signature Identifies Cyclin B1/CDK1 as a Druggable Target to Overcome Natural Killer Cell Dysfunction and Tumor Invasiveness in Melanoma.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Enhancing sensitivity to oxaliplatin in tongue squamous cell carcinoma: mechanistic insights and therapeutic potential of DHA combination therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- CDK1-driven phosphorylation networks promote glioblastoma progression via MAP1B-mediated microtubule destabilization.Frontiers in oncology · 2025Article
- Mathematical strategies for predicting resistant subpopulations from scRNAseq data of a PANC-1 3D tissue model: Insight into gemcitabine resistance and TGFB1-induced invasion and EMT.Computational and structural biotechnology journal · 2025Article
- GETgene-AI: a framework for prioritizing actionable cancer drug targets.Frontiers in systems biology · 2025Article
- [Expression and its clinical significance of cell-cycle dependent kinase 1 in malignant peripheral nerve sheath tumors].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2024Article
- Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPancreatic cancer stem cells (CSCs) promote pancreatic ductal adenocarcinoma (PDAC) tumorigenesis and chemoresistance. Cyclin-dependent kinase 1 (CDK1) plays an important role in tumor initiation in other tumors, but the function of CDK1 in PDAC remains unclear. Fisetin is a bioactive flavonoid with anti-tumor properties in multiple tumors, while its function in CSCs remains elusive.
resultsIn this study, we demonstrated that CDK1 was correlated with prognosis and was highly expressed in pancreatic cancer tissue and gemcitabine-resistant cells. Silencing CDK1 impaired tumor stemness and reduced a subset of CSCs. We found that fisetin blocked the kinase pocket domain of CDK1 and inhibited pancreatic CSC characteristics. Using acetylation proteomics analysis and phosphorylation array assay, we confirmed that fisetin reduced CDK1 expression and increased CDK1 acetylation at lysine 33 (K33), which resulted in the suppression of CDK1 phosphorylation. Silencing CDK1 or STAT3 suppressed tumor stemness properties, while overexpressing CDK1 or STAT3 showed the opposite effect. Mutation or acetylation of CDK1 at K33 weakened STAT3 phosphorylation at Y705, impairing the expression of stem-related genes and pancreatic cancer stemness. In addition, lack of histone deacetylase 3 (HDAC3), which deacetylates CDK1, contributed to weakening STAT3 phosphorylation by regulating the post-translational modification of CDK1, thereby decreasing the stemness of PDAC. Moreover, our results revealed that fisetin enhanced the effect of gemcitabine through eliminating a subpopulation of pancreatic CSCs by inhibiting the CDK1-STAT3 axis in vitro and in vivo.
conclusionOur findings highlight the role of post-translational modifications of CDK1-STAT3 signaling in maintaining cancer stemness of PDAC, and indicated that targeting the CDK1-STAT3 axis with inhibitors such as fisetin is a potential therapeutic strategy to diminish drug resistance and eliminate PDAC.
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