ArticleCancer medicine2019
Study of the mechanism by which dinaciclib induces apoptosis and cell cycle arrest of lymphoma Raji cells through a CDK1-involved pathway.
Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 37 citations in OpenAlex.
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- Novel meriolin derivatives potently inhibit cell cycle progression and transcription in leukemia and lymphoma cells via inhibition of cyclin-dependent kinases (CDKs).Cell death discovery · 2024Article
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- Recent Progress in CDK4/6 Inhibitors and PROTACs.Molecules (Basel, Switzerland) · 2023Review
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- The Critical Role of 12-Methyl Group of Anthracycline Dutomycin to Its Antiproliferative Activity.Molecules (Basel, Switzerland) · 2022Article
- Cyclin-dependent kinase inhibitors exert distinct effects on patient-derived 2D and 3D glioblastoma cell culture models.Cell death discovery · 2021Article
- Bioinformatics analysis shows that TOP2A functions as a key candidate gene in the progression of cervical cancer.Biomedical reports · 2020Article
- Gamma-irradiation degraded sulfated polysaccharide from a new red algal strainOncology letters · 2020Article
- Extracellular Vesicle Delivery of TRAIL Eradicates Resistant Tumor Growth in Combination with CDK Inhibition by Dinaciclib.Cancers · 2020Article
- Study of the mechanism by which dinaciclib induces apoptosis and cell cycle arrest of lymphoma Raji cells through a CDK1-involved pathway.Cancer medicine · 2019Article
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8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to identify and evaluate the mechanism by which apoptosis and cell cycle arrest were induced by dinaciclib in lymphoma Raji cells.
methodsThe colony formation assay was used to detect cell proliferation of Raji cells. Cell cycle arrest and cell apoptosis were determined by flow cytometry and TUNEL assays, respectively. Protein expression related to the Raji cell state was evaluated by Western blot. The Raji/Dinaciclib drug-resistant cell line was established, where the regulating functions of CDK1-involved pathway were verified. In addition, the effect of dinaciclib in vivo was examined in orthotopically implanted tumors in nude mice.
resultsCell apoptosis was induced, and DNA synthesis ability was decreased in a time-dependent manner in dinaciclib-treated lymphoma Raji cells. Furthermore, the cell cycle was found to be blocked in the G2/M Phase. Further study indicated that CDK1-involved pathway played a key regulatory role in this process. It was revealed by cell transfection that the expression of cell cycle proteins was downregulated after treatment with dinaciclib through a CDK1-involved pathway, which eventually led to apoptosis. Knockdown of CDK1 restored the sensitivity of the Raji/Dinaciclib cells to dinaciclib. Xenograft model of nude mice showed that dinaciclib treatment in vivo could effectively inhibit tumor growth, consistent with the experiment results mentioned before.
conclusionIn this study, we clarified the mechanisms through which dinaciclib induces Raji cell apoptosis and blocks the cell cycle through a CDK1-involved pathway, which supported that dinaciclib had potential values in the treatment of lymphoma.
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