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TPX2 serves as a novel target for expanding the utility of PARPi in pancreatic cancer through conferring synthetic lethality.
Gut
November 2024
Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China
Article Synopsis
- PARP inhibitors have been approved for maintenance therapy in metastatic pancreatic cancer patients with rare BRCA1/2 mutations, highlighting a significant unmet need for broader applications.* -
- Research involved RNA sequencing to identify potential targets for PARPi sensitivity, verifying that targeting TPX2 can increase vulnerability to these inhibitors and promote synthetic lethality in various cancer models.* -
- TPX2 plays a crucial role in the DNA repair process, and manipulating its phosphorylation status enhances PARPi sensitivity and contributes to genomic instability, suggesting that combining TPX2 inhibition with other therapies like gemcitabine could improve treatment effectiveness.*
Aurora A and cortical flows promote polarization and cytokinesis by inducing asymmetric ECT-2 accumulation.
Elife
December 2022
Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, United States.
In the early embryo, cell polarization and cytokinesis are interrelated yet distinct processes. Here, we sought to understand a poorly understood aspect of cleavage furrow positioning. Early embryos deficient in the cytokinetic regulator centralspindlin form furrows, due to an inhibitory activity that depends on aster positioning relative to the polar cortices.
View Article and Find Full Text PDFCtIP Regulates Mitotic Spindle Assembly by Modulating the TPX2-Aurora A Signaling Axis.
Cells
September 2022
Laboratory of Genomic Instability and Cancer Therapeutics, Cancer Mutation Research Center, School of Medicine, Chosun University, 375 Seosuk-dong, Gwangju 61452, Korea.
CtBP-interacting protein (CtIP) plays a critical role in controlling the homologous recombination-mediated DNA double-stranded break (DSB) repair pathway through DNA end resection, and recent studies suggest that it also plays a role in mitosis. However, the mechanism by which CtIP contributes to mitosis regulation remains elusive. Here, we show that depletion of CtIP leads to a delay in anaphase progression resulting in misaligned chromosomes, an aberrant number of centrosomes, and defects in chromosome segregation.
View Article and Find Full Text PDFPolo-like kinase-1, Aurora kinase A and WEE1 kinase are promising druggable targets in CML cells displaying BCR::ABL1-independent resistance to tyrosine kinase inhibitors.
Front Oncol
August 2022
Dipartimento di Medicina Specialistica, Diagnostica e Sperimentale Università di Bologna, Bologna, Italy.
Article Synopsis
- In chronic myeloid leukemia (CML), the dysregulated activity of Aurora kinase A and PLK1 is linked to resistance to imatinib and persistent leukemic stem cells, potentially leading to more severe disease progression.
- A new treatment strategy involving the combination of inhibitors for Aurora kinase A or PLK1 (danusertib or volasertib) with a WEE1 inhibitor (AZD1775) shows promise by significantly enhancing apoptosis and reducing cell viability in both TKI-sensitive and TKI-resistant CML cell lines.
- This combination therapy demonstrated a notable reduction in the clonogenic potential of CD34+ CML progenitors from patients with advanced disease, suggesting new avenues for improving treatment outcomes for those with multi-T
Combined inhibition of Aurora-A and ATR kinase results in regression of -amplified neuroblastoma.
Nat Cancer
March 2021
Theodor Boveri Institute, Department of Biochemistry and Molecular Biology, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Amplification of is the driving oncogene in a subset of high-risk neuroblastoma. The MYCN protein and the Aurora-A kinase form a complex during S phase that stabilizes MYCN. Here we show that MYCN activates Aurora-A on chromatin, which phosphorylates histone H3 at serine 10 in S phase, promotes the deposition of histone H3.
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