ArticleCancer research2015
CDK2 Inhibition Causes Anaphase Catastrophe in Lung Cancer through the Centrosomal Protein CP110.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Cyclins and Cyclin-Dependent Kinases: Structure, Biological Functions, and Innovative Targeting Strategies in Cancer.MedComm · 2026Review
- Inhibition of cyclin-dependent kinases 12/13 using CT7439 as a treatment for colorectal cancer with CDK12 upregulation.Molecular oncology · 2026Article
- Unlocking ESCC Progression: CCL15-CCR1 Axis Activates AKT/ERK1/2/c-Jun/CDK2 Pathway.Journal of Cancer · 2025Article
- Development of a novel centrosome-related risk signature to predict prognosis and treatment response in lung adenocarcinoma.Discover oncology · 2024Article
- CDK2 inhibition disorders centrosome stoichiometry and alters cellular outcomes in aneuploid cancer cells.Cancer biology & therapy · 2023Article
- lncRNA XIST/miR‑129‑2‑3p axis targets CCP110 to regulate the proliferation, invasion and migration of endometrial cancer cells.Experimental and therapeutic medicine · 2023Article
- Molecular subtypes based on centrosome-related genes can predict prognosis and therapeutic responsiveness in patients with low-grade gliomas.Frontiers in oncology · 2023Article
- Keep Calm and Carry on with Extra Centrosomes.Cancers · 2022Review
- NEDD8-activating enzyme inhibition induces cell cycle arrest and anaphase catastrophe in malignant T-cells.Oncotarget · 2021Article
- Cyclin E in normal physiology and disease states.Trends in cell biology · 2021Review
- Epigenetically Mediated Ciliogenesis and Cell Cycle Regulation, and Their Translational Potential.Cells · 2021Review
- A Novel CDK2/9 Inhibitor CYC065 Causes Anaphase Catastrophe and Represses Proliferation, Tumorigenesis, and Metastasis in Aneuploid Cancers.Molecular cancer therapeutics · 2021Article
- LINC00511 influences cellular proliferation through cyclin-dependent kinases in papillary thyroid carcinoma.Journal of Cancer · 2020Article
- TRIGGERING ANAPHASE CATASTROPHE TO COMBAT ANEUPLOID CANCERS.Transactions of the American Clinical and Climatological Association · 2020Article
- Targeting centrosome amplification, an Achilles' heel of cancer.Biochemical Society transactions · 2019Review
- Adaptively capturing the heterogeneity of expression for cancer biomarker identification.BMC bioinformatics · 2018Article
- Engaging Anaphase Catastrophe Mechanisms to Eradicate Aneuploid Cancers.Molecular cancer therapeutics · 2018Review
- PolyC-binding proteins enhance expression of the CDK2 cell cycle regulatory protein via alternative splicing.Nucleic acids research · 2018Article
- Polo-like kinase 4 inhibition produces polyploidy and apoptotic death of lung cancers.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Regulation of the cell cycle and centrosome biology by deubiquitylases.Biochemical Society transactions · 2017Review
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Authors and funding
21 authors at 2 institutions in 1 country.
Funding
Abstract
Aneuploidy is frequently detected in human cancers and is implicated in carcinogenesis. Pharmacologic targeting of aneuploidy is an attractive therapeutic strategy, as this would preferentially eliminate malignant over normal cells. We previously discovered that CDK2 inhibition causes lung cancer cells with more than two centrosomes to undergo multipolar cell division leading to apoptosis, defined as anaphase catastrophe. Cells with activating KRAS mutations were especially sensitive to CDK2 inhibition. Mechanisms of CDK2-mediated anaphase catastrophe and how activated KRAS enhances this effect were investigated. Live-cell imaging provided direct evidence that following CDK2 inhibition, lung cancer cells develop multipolar anaphase and undergo multipolar cell division with the resulting progeny apoptotic. The siRNA-mediated repression of the CDK2 target and centrosome protein CP110 induced anaphase catastrophe of lung cancer cells. In contrast, CP110 overexpression antagonized CDK2 inhibitor-mediated anaphase catastrophe. Furthermore, activated KRAS mutations sensitized lung cancer cells to CDK2 inhibition by deregulating CP110 expression. Thus, CP110 is a critical mediator of CDK2 inhibition-driven anaphase catastrophe. Independent examination of murine and human paired normal-malignant lung tissues revealed marked upregulation of CP110 in malignant versus normal lung. Human lung cancers with KRAS mutations had significantly lower CP110 expression as compared with KRAS wild-type cancers. Thus, a direct link was found between CP110 and CDK2 inhibitor antineoplastic response. CP110 plays a mechanistic role in response of lung cancer cells to CDK2 inhibition, especially in the presence of activated KRAS mutations.
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