We used breast cancer (HCC1569, HCC1954, BT549, MDA-MB-415, HCC202, MCF7, T47D, CAL51), ovarian cancer (KOC-7C, SKOV3, HEYC2, COLO704, RMG-1, KK, ES-2, EFO21, MCAS, A2780, OV167, PEA2, TOV-21G, OV90, OV207, Kuramochi, OVISE, OVMANA, PEO6, CaOv-3, OV177, OVCAR3, OVCAR5, OVSAHO, OVTOKO, PEO14), colorectal cancer (HCT-116, HCT-15, DLD-1, COLO 205, COLO320DM, COLO320HSR, NCI-H747, NCI-H716, COLO201, LS1034, SNU-C2B, SNU-C1, LS513, LS411N, ATR-FLOX, LS174t, WiDr, RKO, SK-CO1, HCT-8, LS-180, HT-29, C2Bbe1, SW480), and immortalized breast epithelial (MCF-10–2A, MCF-12A) cell lines from the American Type Culture Collection (ATCC) or the Deutsche Sammlung von Mikroorganismen und Zellkulturen (DSMZ) for our experiments grown as described elsewhere (42 (link)–44 (link, link)). Cultured cells were synchronized as needed by using single or double thymidine blockade. For experiments with CFI-400945, the PLK4 inhibitor was added to medium at 10 nM, 50 nM, 100 nM, or 500 nM concentrations and compared with results with DMSO controls.