ArticleAmerican journal of translational research2021
TANK-binding kinase 1 inhibitor GSK8612 enhances daunorubicin sensitivity in acute myeloid leukemia cells via the AKT-CDK2 pathway.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Design and Synthesis of Novel Isoflavene TANK-Binding Kinase 1 Inhibitors With Anti-Inflammatory Activity.ChemMedChem · 2026Article
- Expression patterns, prognostic significance, and immune correlations of the TNFAIP8 family in acute myeloid leukemia: a comprehensive bioinformatics analysis.Discover oncology · 2025Article
- A review on the role of cyclin dependent kinases in cancers.Cancer cell international · 2022Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIt has been established in previous studies that TANK-binding kinase 1 (TBK1) is upregulated in malignant tumors and is therefore associated with poor prognosis. However, the role of TBK1 in acute myeloid leukemia (AML) remains unclear. In this study, we investigated the expression levels and the function of TBK1 in AML.
methodsFirst, TBK1 expression was detected and analyzed using Western blot and qRT-PCR. Then, GSK8612, a novel TBK1 inhibitor, and TBK1-specific siRNA (si-TBK1) were used to inhibit TBK1 function and expression. The effects of TBK1 inhibition on AML were investigated first through a cell counting kit (CCK-8) assay, followed by trypan blue staining to assess cell apoptosis and cell cycle progression
resultsWe found a significantly higher TBK1 expression in AML patients with poor prognoses. GSK8612 successfully inhibited TBK1 expression, resulting in the increased sensitivity of AML cells to daunorubicin. Mechanistically, TBK1 inhibition (by GSK8612 and si-TBK1) regulated cyclin-dependent kinase 2 (CDK2) levels in AML cells via the AKT pathway. Moreover, it was observed that the inhibition of protein kinase B (AKT) activity also resulted in the increased sensitivity of AML cell lines to daunorubicin, validating the relationship between TBK1 and the AKT-CDK2 pathway. Similar results were obtained in MNCs from patients with AML.
conclusionTBK1 is a potential prognostic factor for AML, and its inhibition may improve the sensitivity of AML cells to daunorubicin. This regulatory effect is predicted to involve the TBK1-AKT-CDK2 pathway.
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35035703PMC8748083W4206846188What OpenQuestion holds
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