TY - JOUR
AU - Klotz, Daniel Martin
AU - Schwarz, Franziska Maria
AU - Dubrovska, Anna
AU - Schuster, Kati
AU - Theis, Mirko
AU - Krüger, Alexander
AU - Kutz, Oliver
AU - Link, Theresa
AU - Wimberger, Pauline
AU - Drukewitz, Stephan
AU - Buchholz, Frank
AU - Thomale, Jürgen
AU - Kuhlmann, Jan Dominik
TI - Establishment and Molecular Characterization of an In Vitro Model for PARPi-Resistant Ovarian Cancer.
JO - Cancers
VL - 15
IS - 15
SN - 2072-6694
CY - Basel
PB - MDPI
M1 - DKFZ-2023-01644
SP - 3774
PY - 2023
AB - Overcoming PARPi resistance is a high clinical priority. We established and characterized comparative in vitro models of acquired PARPi resistance, derived from either a BRCA1-proficient or BRCA1-deficient isogenic background by long-term exposure to olaparib. While parental cell lines already exhibited a certain level of intrinsic activity of multidrug resistance (MDR) proteins, resulting PARPi-resistant cells from both models further converted toward MDR. In both models, the PARPi-resistant phenotype was shaped by (i) cross-resistance to other PARPis (ii) impaired susceptibility toward the formation of DNA-platinum adducts upon exposure to cisplatin, which could be reverted by the drug efflux inhibitors verapamil or diphenhydramine, and (iii) reduced PARP-trapping activity. However, the signature and activity of ABC-transporter expression and the cross-resistance spectra to other chemotherapeutic drugs considerably diverged between the BRCA1-proficient vs. BRCA1-deficient models. Using dual-fluorescence co-culture experiments, we observed that PARPi-resistant cells had a competitive disadvantage over PARPi-sensitive cells in a drug-free medium. However, they rapidly gained clonal dominance under olaparib selection pressure, which could be mitigated by the MRP1 inhibitor MK-751. Conclusively, we present a well-characterized in vitro model, which could be instrumental in dissecting mechanisms of PARPi resistance from HR-proficient vs. HR-deficient background and in studying clonal dynamics of PARPi-resistant cells in response to experimental drugs, such as novel olaparib-sensitizers.
KW - PARPi resistance (Other)
KW - cisplatin (Other)
KW - ovarian cancer (Other)
LB - PUB:(DE-HGF)16
C6 - pmid:37568590
C2 - pmc:PMC10417418
DO - DOI:10.3390/cancers15153774
UR - https://inrepo02.dkfz.de/record/278410
ER -