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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: The disruption of the CCDC6 – PP4 axis induces a BRCAness like phenotype and sensitivity to PARP inhibitors in high-grade serous ovarian carcinoma

Fig. 5

CCDC6 protein levels evaluation in Patient Derived Xenograft (PDX) and in naturally occurring CCDC6-null and CCDC6-competent HGSOC models. A MNHOC 239, MNHOC 266, and MNHOC 124 PDX samples were immunostained with an anti-CCDC6 antibody. IHC analysis revealed a diffuse positivity in all the analysed samples with negligible differences between them. ([S]: cisplatin sensitive; [R]: cisplatin resistant). B CCDC6 IHC expression on PDX samples was quantified on digital glass slides and reported as Optical Density (OD) arbitrary units. The graph shows Nuclear and Cytoplasmatic CCDC6 expression in each analysed sample. C CCDC6 protein expression levels in PEO1 and PEO4 cells are shown by anti-CCDC6 and anti-tubulin immunoblots. D CCDC6 relative mRNA expression in PEO1 and PEO4 cells as evaluated by quantitative RT-PCR. E Olaparib and Cisplatin sensitivity in CCDC6-naturally null PEO1 cells and in CCDC6-proficient PEO4 cells have been evaluated. The rescue with myc-CCDC6 in PEO1 cells (CCDC6 +) and the silencing by ShCCDC6 in PEO4 cells, modulated the drugs sensitivity with respect to controls (EV or ShCTRL). IC50 values and surviving fractions are displayed. F CI values according to 1:2 concentration ratio of Cisplatin and Olaparib and the Dose Reduction Index (DRI) for each drug are reported in the tables. In the PEO4 cells, following CCDC6 depletion, the DRI resulted > 1, as the dose of Olaparib and Cisplatin to obtain the 50% Fractional Effect (IC50) resulted reduced. Error bars indicate the standard error mean derived from three independent experiments

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