Eskiler, Gamze GüneyÇeçener, GülşahEgeli, ÜnalTunca, Berrin2024-07-102024-07-102019-05-011095-6670https://doi.org/10.1002/jbt.22286https://onlinelibrary.wiley.com/doi/10.1002/jbt.22286https://hdl.handle.net/11452/43108The objective of the present study was to elucidate the effect of BMN 673 (talozoparib) on BRCA1 mutant (HCC1937) and wild-type (MDA-MB-231) triple negative breast cancer (TNBC). The in vitro cytotoxicity results indicated that BMN 673 had considerable inhibitory effects on HCC1937 and MDA-MB-231 cell lines by inducing apoptosis, multicaspase activity, G2/M arrest, and altering the expression levels of apoptosis-related genes (P < 0.01). Additionally, BMN 673 indicated no toxicity on MCF-10A control cells until a certain concentration and incubation time. However, BMN 673, a novel and selective poly ADP ribose polymerase inhibitor, was more potent in TNBC cells bearing BRCA1 mutant than those with wild-type BRCA1. In conclusion, our study, for the first time, demonstrated a molecular mechanism of the induction of apoptosis by BMN 673 in TNBC with different genetic profile. However, further investigations regarding the exact molecular mechanisms underlying BMN 673-inducing apoptotic death and gene-cell line associations are required.eninfo:eu-repo/semantics/closedAccessSynthetic lethalityVivo sensitivityDna-repairCell-linesMechanismsBrca1Apoptotic deathBmn 673 (talozoparib)BrcaTriple negative breast cancerBiochemistry & molecular biologyToxicologyArticle00046732790000633510.1002/jbt.22286