Poly (ADP-ribose) polymerase inhibitors (PARPi) have proven to be beneficial to patients with metastatic
breast cancer with BRCA1/2 (
BReast CAncer type 1 and type 2 genes) mutations. However, certain PARPi in pre-clinical studies have been shown to inhibit cell growth and promote the death of
breast cancer cells lacking mutations in BRCA1/2. Here, we examined the inhibitory potency of 13 different PARPi in 12
breast cancer cell lines with and without BRCA-mutations using cell viability assays. The results showed that 5 of the 8
triple-negative breast cancer (TNBC) cell lines were susceptible to PARPi regardless of the BRCA-status. The
estrogen receptor (ER) negative/
human epidermal growth factor receptor 2 (HER2) positive (ER-/HER2+) cells, SKBR3 and JIMT1, showed high sensitivity to
Talazoparib. Especially JIMT1, which is known to be resistant to
trastuzumab, was responsive to
Talazoparib at 0.002 µM.
Niraparib,
Olaparib, and
Rucaparib also demonstrated effective inhibitory potency in both advanced TNBC and ER-/HER2+ cells with and without BRCA-mutations. In contrast, a BRCA-mutant TNBC line, HCC1937, was less sensitive to
Talazoparib,
Niraparib,
Rucaparib, and not responsive to
Olaparib. Other PARPi such as UPF1069,
NU1025,
AZD2461, and PJ34HCl also showed potent inhibitory activity in specific
breast cancer cells. Our data suggest that the benefit of PARPi
therapy in
breast cancer is beyond the BRCA-mutations, and equally effective on metastatic TNBC and ER-/HER2+ breast
cancers.