ArticleScientific reports2020
Dinaciclib, a cyclin-dependent kinase inhibitor, suppresses cholangiocarcinoma growth by targeting CDK2/5/9.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 87 citations in OpenAlex.
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- Integrating machine learning and spatiotemporal transcriptomics to build a diagnostic model for osteosarcoma metastasis and to decipher the role of necroptosis genes.Discover oncology · 2026Article
- Focal Adhesion and Cancer Cell Cycle-Associated Resistance.ACS omega · 2026Review
- A novel interpretable machine learning framework integrating clinicopathological and radiomic features for early recurrence prediction in mass-forming intrahepatic cholangiocarcinoma.Cancer imaging : the official publication of the International Cancer Imaging Society · 2026Article
- Genomic and transcriptomic insights into aflatoxin-induced intrahepatic cholangiocarcinoma: an integrated pathway and meta-analysis study.Frontiers in genetics · 2026Article
- Fadraciclib, a CDK2/CDK9 inhibitor, shows efficacy in biliary tract cancer and synergistic potential with olaparib and JQ1 based on MCL1 expression.Cell communication and signaling : CCS · 2025Article
- Chrono-Pharmacology for Cancer: Harnessing Circadian Regulations of the Cell Cycle and Immune Response Dynamics for Precision Therapy.ACS pharmacology & translational science · 2025Review
- Artificial intelligence in the diagnosis and prognosis of intrahepatic cholangiocarcinoma: Applications and challenges.World journal of gastrointestinal oncology · 2025Review
- Combinatorial therapy regimens targeting preclinical models of melanoma resistant to immune checkpoint blockade.The Journal of clinical investigation · 2025Article
- Comprehensive Proteomics Metadata and Integrative Web Portals Facilitate Sharing and Integration of LINCS Multiomics Data.Molecular & cellular proteomics : MCP · 2025Article
- The CDK12-BRCA1 signaling axis mediates dinaciclib-associated radiosensitivity through p53-mediated cellular senescence.Molecular oncology · 2025Article
- CDK4/6 inhibitors upregulate cIAP1/2, and Smac mimetic LCL161 enhances their antitumor effects in cholangiocarcinoma cells.Scientific reports · 2025Article
- Insights into Novel Arylazopyrazolo[1,5-ACS omega · 2025Article
- Bioactive Fused Pyrazoles Inspired by the Adaptability of 5-Aminopyrazole Derivatives: Recent Review.Molecules (Basel, Switzerland) · 2025Review
- Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025Review
- CDK2 inhibition sensitizes anthracycline-induced immunogenic cell death and enhances the efficacy of anti-PD-1 therapy.Frontiers in immunology · 2025Article
- Novel Small Molecule Inhibitors of Cyclin-dependent Kinases as Anticancer Agents.Current medicinal chemistry · 2025Review
- The Cdk inhibitor dinaciclib as a promising anti-tumorigenic agent in biliary tract cancer.Cancer biology & therapy · 2024Article
- A 3D Bioprinted Human Neurovascular Unit Model of Glioblastoma Tumor Growth.Advanced healthcare materials · 2024Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Cholangiocarcinoma (CCA) is a highly invasive cancer, diagnosed at an advanced stage, and refractory to surgical intervention and chemotherapy. Cyclin-dependent kinases (CDKs) regulate cell cycle progression and transcriptional processes, and are considered potential therapeutic targets for cancer. Dinaciclib is a small molecule multi-CDK inhibitor targeting CDK 2/5/9. In this study, the therapeutic efficacy of dinaciclib was assessed using patient-derived xenograft cells (PDXC) and CCA cell lines. Treatment with dinaciclib significantly suppressed cell proliferation, induced caspase 3/7 levels and apoptotic activity in PDXC and CCA cell lines. Dinaciclib suppressed expression of its molecular targets CDK2/5/9, and anti-apoptotic BCL-XL and BCL2 proteins. Despite the presence of cyclin D1 amplification in the PDXC line, palbociclib treatment had no effect on cell proliferation, cell cycle or apoptosis in the PDXC as well as other CCA cell lines. Importantly, dinaciclib, in combination with gemcitabine, produced a robust and sustained inhibition of tumor progression in vivo in a PDX mouse model, greater than either of the treatments alone. Expression levels of two proliferative markers, phospho-histone H3 and Ki-67, were substantially suppressed in samples treated with the combination regimen. Our results identify dinaciclib as a novel and potent therapeutic agent alone or in combination with gemcitabine for the treatment of CCA.
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Registered trials
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