Aurora kinase inhibitors

Kitzen, Jos; Jonge, Maja J.A. de; Verweij, Jaap

doi:10.1016/j.critrevonc.2009.03.009

Cited by 84 publications

(77 citation statements)

References 61 publications

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“…Aurora kinase A (AURKA) has been implicated in numerous types of cancer, including colonic, breast, liver, gastric, uterine, ovarian, non-small cell lung, pancreatic and esophageal cancer (5)(6)(7)(8)(9)(10). Furthermore, a correlation has been observed between the overexpression of AURKA mRNA and tumor progression and shortened survival in patients with HNSCC (11).…”

Section: Introductionmentioning

confidence: 99%

AURKA promotes cell migration and invasion of head and neck squamous cell carcinoma through regulation of the AURKA/Akt/FAK signaling pathway

Yang

Shan

et al. 2016

Oncology Letters

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Abstract. The present study aimed to investigate the mechanism by which Aurora kinase A (AURKA) promotes cell migration and invasion in head and neck squamous cell carcinoma (HNSCC). Transwell assays were performed to investigate the cell migration and invasion abilities of AURKA, whilst western blotting was used to analyze the protein expression in FaDu and Hep2 cells, each treated with pharmacological inhibitors. Following the inhibition of AURKA, Akt and focal adhesion kinase (FAK), the migration and invasion of the FaDu and Hep2 cells decreased. The expression of phosphorylated (p)-AURKA and p-FAK (Y397) was observed to decrease following FaDu and Hep2 cell treatment with VX-680, a small molecular inhibitor of AURKA. The expression of p-Akt and p-FAK (Y397) ceased following treatment with the Akt inhibitor triciribine. The expression of p-FAK (Y397) decreased, however, p-Akt expression did not change following treatment with the FAK inhibitor TAE226. In conclusion, AURKA activates FAK through the AURKA/Akt/FAK signaling pathway, promoting the migration and invasion of HNSCC cells, which may subsequently provide a novel approach for the treatment of HNSCC.

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Section: Introductionmentioning

confidence: 99%

AURKA promotes cell migration and invasion of head and neck squamous cell carcinoma through regulation of the AURKA/Akt/FAK signaling pathway

Yang

Shan

et al. 2016

Oncology Letters

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“…In humans, the Aurora kinases A and B appear to have a central role in this process, including responsibilities for centrosome duplication, alignment of chromosomes and mitotic checkpoint arrest. 137 Overexpression of these kinases can be oncogenic, but inhibition can lead to aberrant mitosis resulting in mitotic catastrophe in the leukemia cells.…”

Section: Aurora Kinase Inhibitorsmentioning

confidence: 99%

Seeking the causes and solutions to imatinib-resistance in chronic myeloid leukemia

2010

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Although only 5000 new cases of chronic myeloid leukemia (CML) were seen in the United States in 2009, this neoplasm continues to make scientific headlines year-after-year. Advances in understanding the molecular pathogenesis coupled with exciting developments in both drug design and development, targeting the initiating tyrosine kinase, have kept CML in the scientific limelight for more than a decade. Indeed, imatinib, a small-molecule inhibitor of the leukemia-initiating Bcr-Abl tyrosine kinase, has quickly become the therapeutic standard for newly diagnosed chronic phase-CML (CP-CML) patients. Yet, nearly one-third of patients will still have an inferior response to imatinib, either failing to respond to primary therapy or demonstrating progression after an initial response. Significant efforts geared toward understanding the molecular mechanisms of imatinib resistance have yielded valuable insights into the cellular biology of drug trafficking, enzyme structure and function, and the rational design of novel small molecule enzyme inhibitors. Indeed, new classes of kinase inhibitors have recently been investigated in imatinibresistant CML. Understanding the pathogenesis of tyrosine kinase inhibitor resistance and the molecular rationale for the development of second and now third generation therapies for patients with CML will be keys to further disease control over the next 10 years.

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“…Several kinase inhibitors were developed and their potential against various cancers have been described during different phases of treatment [6,7].…”

Section: Introductionmentioning

confidence: 99%

Electrochemical and spectrophotometric characterisation of protein kinase inhibitor and anticancer drug danusertib

Popa

Diculescu

2013

Electrochimica Acta

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 2 AbstractThe electrochemical oxidation mechanism of the anti-cancer drug and kinases inhibitor danusertib was studied by cyclic, differential pulse, square wave voltammetry and a glassy carbon electrode. Danusertib undergoes oxidation in a cascade mechanism and depending on the pH of the supporting electrolyte several oxidation peaks were observed. The number of electrons and protons involved in each oxidation step as well as the pK a ~ 10.0 were determined. The analytical determination of danusertib was carried out in pH = 7.0 by square wave voltammetry with LOD = 27.4 nM and UV-VIS spectrophotometry with LOD = 0.5 µM. Different electroactive centres of danusertib were identified through comparative studies with similar compounds such as imatinib and piperazine, and an oxidation mechanism of danusertib proposed.

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Aurora kinase inhibitors

Cited by 84 publications

References 61 publications

AURKA promotes cell migration and invasion of head and neck squamous cell carcinoma through regulation of the AURKA/Akt/FAK signaling pathway

AURKA promotes cell migration and invasion of head and neck squamous cell carcinoma through regulation of the AURKA/Akt/FAK signaling pathway

Seeking the causes and solutions to imatinib-resistance in chronic myeloid leukemia

Electrochemical and spectrophotometric characterisation of protein kinase inhibitor and anticancer drug danusertib

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