Object's details: 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, Sonata Bis 2019/34/E/NZ7/00056, Sonata Bis-9 (dataset)

Provider:Repozytorium Uniwersytetu Łódzkiego

Description

Title:
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, Sonata Bis 2019/34/E/NZ7/00056, Sonata Bis-9 (dataset)
Creator:
Rogalska, Aneta
Contributor:
Department of Medical Biophysics, Institute of Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Poland
Description:
The data set (ZIP file) has been divided into appropriate subfolders with measurement results for: 1. Growth Curve and Population Doubling Time (NCN Sonata Bis 2019_34_E_NZ7_00056) - MS Excel file with raw data + MS Word file with detailed description of the methodology and experiment conditions; 2. Cell Viability - MTT Assay (NCN Sonata Bis 2019_34_E_NZ7_00056) - MS Excel files with raw data: dose respone curve, drugs combination, drugs combination with MDR1 inhibition + MS Word file with detailed description of the methodology and experiment conditions; 3. Clonogenic Assay (NCN Sonata Bis 2019_34_E_NZ7_00056) - MS Excel file with raw data + MS Word file with detailed description of the methodology and experiment conditions + JPG images; 4. Cell Morphology Changes (NCN Sonata Bis 2019_34_E_NZ7_00056) - MS Word file with detailed description of the methodology and experiment conditions + TIF images; 5. Western Blotting (NCN Sonata Bis 2019_34_E_NZ7_00056) ) - MS Excel file with raw data + MS Word file with detailed description of the methodology and experiment conditions + TIF images; 6. Immunofluorescence analysis of gammaH2AX and RAD51 foci formation (NCN Sonata Bis 2019_34_E_NZ7_00056) - MS Word file with detailed description of the methodology and experiment conditions + LIF images; 7. Neutral Comet Assay (NCN Sonata Bis 2019_34_E_NZ7_00056) - MS Excel file with raw data + MS Word file with detailed description of the methodology and experiment conditions + TIF images; 8. Chromosomal Structural Aberrations (NCN Sonata Bis 2019_34_E_NZ7_00056) - MS Excel file with raw data + MS Word file with detailed description of the methodology and experiment conditions + PNG images; 9. Cell Cycle and gammaH2AX Staining (NCN Sonata Bis 2019_34_E_NZ7_00056) - MS Excel file with raw data + MS Word file with detailed description of the methodology and experiment conditions.;
The 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. 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.;
This research was funded by the National Science Centre, Poland (Project grant number: Sonata Bis 2019/34/E/NZ7/00056).
Object availability:
free access
Rights:
Uznanie autorstwa 4.0 Międzynarodowe;
http://creativecommons.org/licenses/by/4.0
Date:
2023.04.11;
2020.10.01
Type:
Dataset
Language:
English
Format:
application/octet-stream
Subject:
ovarian cancer;
targeted therapy;
olaparib;
PARP1;
ATR/CHK1 pathway
Identifier: http://hdl.handle.net/11089/46664
Data provider:
Repozytorium Uniwersytetu Łódzkiego

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Object's details: 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, Sonata Bis 2019/34/E/NZ7/00056, Sonata Bis-9 (dataset)

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