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Treatment with onvansertib, a specific PLK1 inhibitor, overcomes olaparib resistance in high-grade serous ovarian carcinoma patient-derived xenografts

ABSTRACT: Treatment with onvansertib, a specific PLK1 inhibitor, overcomes olaparib resistance in high-grade serous ovarian carcinoma patient-derived xenografts

PROVIDER: PRJEB63138 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11552031.fastq.gz	Fastqsanger.gz
	ERR11552032.fastq.gz	Fastqsanger.gz
	ERR11552033.fastq.gz	Fastqsanger.gz
	ERR11552034.fastq.gz	Fastqsanger.gz
	ERR11552035.fastq.gz	Fastqsanger.gz

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Treatment with onvansertib, a specific PLK1 inhibitor, overcomes olaparib resistance in high-grade serous ovarian carcinoma patient-derived xenografts

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Project description:Analysis of enzalutamide- and/or olaparib-responsive gene expression in prostate cancer cells. The hypothesis tested in the present study was that enzalutamide influences the expression of genes that are involved in important bioprocesses in prostate cance rcells, including DNA damage response genes and this effect may synergize with poly(ADP-ribose) polymerase inhibitor olaparib in cytotoxicity to prstate cancer cells. prostate cancer cells were pretreated with enzalutamide or vehicle control DMSO for 24 h, followed by treatment with enzalutamide, olaparib, enzalutamide+olaparib, or vehicle control DMSO for 48 h. Gene expression in enzalutamide+olaparib-treated cells was compared with taht in vehicle control- and single agent-treated cells.

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Activation of Wnt signaling promotes olaparib resistant ovarian cancer.

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Genetic enhancers of partial PLK1 inhibition reveal hypersensitivity to kinetochore perturbations

Project description:Polo-like kinase 1 (PLK1) is a serine/threonine kinase required for mitosis and cytokinesis. As cancer cells are often hypersensitive to partial PLK1 inactivation, chemical inhibitors of PLK1 have been developed and tested in clinical trials. However, these molecules alone were not completely effective. PLK1 promotes numerous molecular and cellular events in the cell division cycle. To date, it is unclear which of these events most crucially depend on PLK1 activity. We used a CRISPR-based genome-wide screening strategy to identify genes whose inactivation enhances cell proliferation defects upon partial chemical inhibition of PLK1. Genes identified encode proteins that are functionally linked to PLK1 in multiple ways. Among them, factors that promote centromere and kinetochore function were clearly enriched. In particular, inactivation of the kinesin KIF18A or SKA1 in PLK1-compromised cells results in mitotic defects, activation of the spindle assembly checkpoint and nuclear reassembly defects. Our results suggest that functions of PLK1 at kinetochores are most sensitive to its inhibition, and point at KIF18A as a possible target for combinatorial therapies using existing PLK1 inhibitors.

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