ArticlePloS one2017
A cyclin-dependent kinase inhibitor, dinaciclib in preclinical treatment models of thyroid cancer.
Article in PloS one, 2017. 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.
- Anaplastic thyroid cancer: Genetic roles, targeted therapy, and immunotherapy.Genes & diseases · 2025Review
- Proapoptotic Bcl-2 inhibitor as potential host directed therapy for pulmonary tuberculosis.Nature communications · 2025Article
- Dinaciclib Interrupts Cell Cycle and Induces Apoptosis in Oral Squamous Cell Carcinoma: Mechanistic Insights and Therapeutic Potential.International journal of molecular sciences · 2025Article
- The Cdk inhibitor dinaciclib as a promising anti-tumorigenic agent in biliary tract cancer.Cancer biology & therapy · 2024Article
- Novel Insights in the Genomics of Anaplastic Thyroid Carcinoma: A Role for Cyclin-Dependent Kinase Inhibition?Cancers · 2023Article
- Article
- Co-targeting CDK2 and CDK4/6 overcomes resistance to aromatase and CDK4/6 inhibitors in ER+ breast cancer.NPJ precision oncology · 2022Article
- Rational drug combination design in patient-derived avatars reveals effective inhibition of hepatocellular carcinoma with proteasome and CDK inhibitors.Journal of experimental & clinical cancer research : CR · 2022Article
- Article
- Pre-therapeutic efficacy of the CDK inhibitor dinaciclib in medulloblastoma cells.Scientific reports · 2021Article
- Article
- Bioinformatics analysis identified CDC20 as a potential drug target for cholangiocarcinoma.PeerJ · 2021Article
- Long noncoding RNAs SET-binding factor 2-antisense RNA1 promotes cell growth through targeting miR-431-5p/CDK14 axis in human papillary thyroid cancer.The Kaohsiung journal of medical sciences · 2020Article
- The differences of regulatory networks between papillary and anaplastic thyroid carcinoma: an integrative transcriptomics study.Cancer biology & therapy · 2020Article
- Down-Regulation of the Mammalian Target of Rapamycin (mTOR) Pathway Mediates the Effects of the Paeonol-Platinum(II) Complex in Human Thyroid Carcinoma Cells and Mouse SW1736 Tumor Xenografts.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Therapeutic Targeting of the General RNA Polymerase II Transcription Machinery.International journal of molecular sciences · 2020Review
- Dinaciclib prolongs survival in theAmerican journal of translational research · 2020Article
- Activation of the Kynurenine Pathway in Human Malignancies Can Be Suppressed by the Cyclin-Dependent Kinase Inhibitor Dinaciclib.Frontiers in immunology · 2020Article
- PES1 promotes BET inhibitors resistance and cells proliferation through increasing c-Myc expression in pancreatic cancer.Journal of experimental & clinical cancer research : CR · 2019Article
- Targeting PLKs as a therapeutic approach to well-differentiated thyroid cancer.Endocrine-related cancer · 2019Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundWe explored the therapeutic effects of dinaciclib, a cyclin-dependent kinase (CDK) inhibitor, in the treatment of thyroid cancer. MATERIALS AND
methodsSeven cell lines originating from three pathologic types of thyroid cancer (papillary, follicular and anaplastic) were studied. The cytotoxicity of dinaciclib was measured using a lactate dehydrogenase assay. The expression of proteins associated with cell cycle and apoptosis was assessed using Western blot analysis and immunofluorescence microscopy. Cell cycle distribution was measured by flow cytometry and immunofluorescence microscopy. Apoptosis and caspase-3 activity were measured by flow cytometry and fluorometric assay. Mice bearing flank anaplastic thyroid cancer (ATC) were treated with intraperitoneal injections of dinaciclib.
resultsDinaciclib inhibited thyroid cancer cell proliferation in a dose-dependent manner. Dinaciclib had a low median-effect dose (≤ 16.0 nM) to inhibit cell proliferation in seven thyroid cancer cell lines. Dinaciclib decreased CDK1, cyclin B1, and Aurora A expression, induced cell cycle arrest in the G2/M phase, and induced accumulation of prophase mitotic cells. Dinaciclib decreased Mcl-1, Bcl-xL and survivin expression, activated caspase-3 and induced apoptosis. In vivo, the growth of ATC xenograft tumors was retarded in a dose-dependent fashion with daily dinaciclib treatment. Higher-dose dinaciclib (50 mg/kg) caused slight, but significant weight loss, which was absent with lower-dose dinaciclib (40 mg/kg) treatment.
conclusionsDinaciclib inhibited thyroid cancer proliferation both in vitro and in vivo. These findings support dinaciclib as a potential drug for further studies in clinical trials for the treatment of patients with refractory thyroid cancer.
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