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Olaparib-Resistant BRCA2MUT Ovarian Cancer Cells with Restored BRCA2 Abrogate Olaparib-Induced DNA Damage and G2/M Arrest Controlled by the ATR/CHK1 Pathway for Survival

dc.contributor.authorBiegała, Łukasz
dc.contributor.authorGajek, Arkadiusz
dc.contributor.authorMarczak, Agnieszka
dc.contributor.authorRogalska, Aneta
dc.date.accessioned2023-05-08T10:34:27Z
dc.date.available2023-05-08T10:34:27Z
dc.date.issued2023
dc.identifier.citationBiegała, Ł.; Gajek, A.; Marczak, A.; Rogalska, A. Olaparib-Resistant BRCA2MUT Ovarian Cancer Cells with Restored BRCA2 Abrogate Olaparib-Induced DNA Damage and G2/M Arrest Controlled by the ATR/CHK1 Pathway for Survival. Cells 2023, 12, 1038. https:/pl_PL
dc.identifier.issn2073-4409
dc.identifier.urihttp://hdl.handle.net/11089/46974
dc.description.abstractThe PARP inhibitor (PARPi) olaparib is currently the drug of choice for serous ovarian cancer (OC), especially in patients with homologous recombination (HR) repair deficiency associated with deleterious BRCA1/2 mutations. Unfortunately, OC patients who fail to respond to PARPi or relapse after treatment have limited therapeutic options. To elucidate olaparib resistance and enhance the efficacy of olaparib, intracellular factors exploited by OC cells to achieve decreased sensitivity to PARPi were examined. An olaparib-resistant OC cell line, PEO1-OR, was established from BRCA2MUT PEO1 cells. The anticancer activity and action of olaparib combined with inhibitors of the ATR/CHK1 pathway (ceralasertib as ATRi, MK-8776 as CHK1i) in olaparib-sensitive and -resistant OC cell lines were evaluated. Whole-exome sequencing revealed that PEO1-OR cells acquire resistance through subclonal enrichment of BRCA2 secondary mutations that restore functional full-length protein. Moreover, PEO1-OR cells upregulate HR repair-promoting factors (BRCA1, BRCA2, RAD51) and PARP1. Olaparib-inducible activation of the ATR/CHK1 pathway and G2/M arrest is abrogated in olaparib-resistant cells. Drug sensitivity assays revealed that PEO1-OR cells are less sensitive to ATRi and CHK1i agents. Combined treatment is less effective in olaparib-resistant cells considering inhibition of metabolic activity, colony formation, survival, accumulation of DNA double-strand breaks, and chromosomal aberrations. However, synergistic antitumor activity between compounds is achievable in PEO1-OR cells. Collectively, olaparib-resistant cells display co-existing HR repair-related mechanisms that confer resistance to olaparib, which may be effectively utilized to resensitize them to PARPi via combination therapy. Importantly, the addition of ATR/CHK1 pathway inhibitors to olaparib has the potential to overcome acquired resistance to PARPi.pl_PL
dc.language.isoenpl_PL
dc.publisherMDPIpl_PL
dc.relation.ispartofseriesCells;12(7), 1038
dc.rightsUznanie autorstwa 4.0 Międzynarodowe*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectovarian cancerpl_PL
dc.subjecttargeted therapypl_PL
dc.subjectolaparibpl_PL
dc.subjectPARP1pl_PL
dc.subjectATR/CHK1 pathwaypl_PL
dc.titleOlaparib-Resistant BRCA2MUT Ovarian Cancer Cells with Restored BRCA2 Abrogate Olaparib-Induced DNA Damage and G2/M Arrest Controlled by the ATR/CHK1 Pathway for Survivalpl_PL
dc.typeArticlepl_PL
dc.page.number38pl_PL
dc.contributor.authorAffiliationDepartment of Medical Biophysics, Institute of Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Polandpl_PL
dc.contributor.authorAffiliationDepartment of Medical Biophysics, Institute of Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Polandpl_PL
dc.contributor.authorAffiliationDepartment of Medical Biophysics, Institute of Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Polandpl_PL
dc.contributor.authorAffiliationDepartment of Medical Biophysics, Institute of Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Polandpl_PL
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dc.identifier.doi10.3390/cells12071038
dc.disciplinenauki biologicznepl_PL


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