Fig. 7

ILK functional inhibition in combination with carboplatin effectively reduces the platinum resistant OCSC phenotype. A-D Tumor morphology, volumes, weights, and numbers of peritoneal metastases derived from HEY-A8 cells injected intraperitoneally in NSG mice treated with DMSO, cpd-22, carboplatin and/or combination (n = 5 per group). Data are shown as means ± s.e.m. Significant differences are marked (N = 5 per group; *P < 0.05, **P < 0.01, ***P < 0.001, and **** P < 0.0001). E Graphical representation of ex vivo single cell characterization. F Spheroid morphology (left panel), CCK-8 proliferation assay and count (right panels) of OC cells isolated from xenografts and grown ex vivo (N = 3; ***P < 0.001 and ****P < 0.0001). G Percentage of ALDH⁺ cells in DMSO control, DMSO + carboplatin-, cpd-22-, cdp-22 + carboplatin-treated xenografts. Cells were isolated by mechanical and enzymatic digestion and ALDH⁺ cells were detected by FACS. H ALDH1A1, Nanog, Sox-2, and Oct-4 mRNA levels measured by qRT-PCR in OC cells isolated from tumors treated with vehicle, cpd-22 alone or in combination with carboplatin (N = 3; *P < 0.05, **P < 0.01, and ****P < 0.0001). I WB for Fzd7, p-ILK^Ser246, ILK, p-AKT^Ser473, AKT, p-BAD^Ser136, Bad, Ccaspase-3, caspase-3, and GAPDH in whole protein extract from single cells isolated from tumors and grown as spheroids (left panel) (N = 3 animals per group). Densitometry quantifies Fzd7 expression levels and p-ILK^Ser246/ILK, p-AKT^Ser473/AKT, p-Bad^Ser136/Bad, and Ccaspase-3/caspase-3 ratio (right panel) (N = 3; *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001)