ArticleInternational journal of hematology2010
p53 is critical for the Aurora B kinase inhibitor-mediated apoptosis in acute myelogenous leukemia cells.
Article in International journal of hematology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 36 citations in OpenAlex.
- Utilizing TP53 hotspot mutations as effective predictors of gemcitabine treatment outcome in non-small-cell lung cancer.Cell death discovery · 2025Article
- Review
- Unmasking the biological function and regulatory mechanism of NOC2L: a novel inhibitor of histone acetyltransferase.Journal of translational medicine · 2023Review
- Chromosomal Instability in Acute Myeloid Leukemia.Cancers · 2021Review
- High-throughput Chemical Screening Identifies Focal Adhesion Kinase and Aurora Kinase B Inhibition as a Synergistic Treatment Combination in Ewing Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Dual Targeting of Aurora Kinases with AMG 900 Exhibits Potent Preclinical Activity Against Acute Myeloid Leukemia with Distinct Post-Mitotic Outcomes.Molecular cancer therapeutics · 2018Article
- Article
- Danusertib, a potent pan-Aurora kinase and ABL kinase inhibitor, induces cell cycle arrest and programmed cell death and inhibits epithelial to mesenchymal transition involving the PI3K/Akt/mTOR-mediated signaling pathway in human gastric cancer AGS and NCI-N78 cells.Drug design, development and therapy · 2015Article
- Article
- Aurora kinases in childhood acute leukemia: the promise of aurora B as therapeutic target.Leukemia · 2013Article
- Article
- Frequency of TP53 Mutations and its Impact on Drug Sensitivity in Acute Myeloid Leukemia?Indian journal of clinical biochemistry : IJCB · 2012Article
- Cell cycle control in acute myeloid leukemia.American journal of cancer research · 2012Article
- Aurora B interacts with NIR-p53, leading to p53 phosphorylation in its DNA-binding domain and subsequent functional suppression.The Journal of biological chemistry · 2011Article
- Aurora kinase inhibitors as anticancer molecules.Biochimica et biophysica actaReview
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously showed that AZD1152-HQPA, the inhibitor of Aurora B kinase potently induced growth arrest and apoptosis of various types of human leukemia cells including MV4-11 acute myelogenous leukemia (AML) cells, although the molecular mechanisms by which this class of kinase inhibitors induces apoptosis remain to be fully elucidated. We have recently established the MV4-11 subline, designated as MV4-11 TP53 R248W, which possesses transcriptionally inactive R248W mutation in the TP53 gene. MV4-11 TP53 R248W cells were relatively resistant to AZD1152-HQPA-mediated growth arrest, as measured by MTT and clonogenic assays. AZD1152-HQPA (10-100 nM, 48 h) strikingly induced apoptosis of MV4-11 cells, as assessed by Annexin V binding, loss of mitochondrial outer membrane potential, and activation of caspase cascade, in parallel with up-regulation of p53 and its target molecules Bax and Noxa. Notably, AZD1152-HQPA (10-100 nM, 48 h) induced polyploidy rather than apoptosis in MV4-11 TP53 R248W cells. The polyploid cells were eventually eliminated via apoptosis at later time period (72-120 h) in association with up-regulation of p73. Taken together, p53 plays an important role in AZD1152-HQPA-induced growth arrest and early onset of apoptosis in AML cells. P73 may mediate the late onset of apoptosis to eliminate the polyploid cells caused by the inhibitor of Aurora B kinase.
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