Fig. 5: ATAD2 targeting results in cell-cycle arrest and apoptosis induction in ovarian cancer cells. | Cell Death & Disease

Fig. 5: ATAD2 targeting results in cell-cycle arrest and apoptosis induction in ovarian cancer cells.

From: ATAD2 is a driver and a therapeutic target in ovarian cancer that functions by upregulating CENPE

Fig. 5

A and C Flow cytometry analysis of ovarian cancer cells, PA-1 (A) and SK-OV3 (C), after treatment with DMSO or 5 µM BAY-850 for 48 h. B and D The percentage of cells in each phase of the cell cycle in PA-1 (B) and SK-OV3 (C) cells from (A, C). E The indicated ovarian cancer cell lines were treated with vehicle or 5 µM BAY-850 for 5 days, and apoptosis was measured via annexin V staining. Relative apoptosis in BAY-850-treated cells is plotted with respect to DMSO-treated cells. F The indicated ovarian cancer cell lines were treated with vehicle or 5 µM BAY-850 for 5 days, and poly (ADP-ribose) polymerase (PARP) cleavage was measured via immunoblotting. ACTINB was used as loading control. G Heatmaps showing alterations in centromere gene expression (based on RNA sequencing data) in both PA-1 and SK-OV3 cells treated with 5 µM BAY-850 for 48 h relative to gene expression in cells treated with DMSO. H Quantitative reverse-transcriptase-polymerase chain reaction (qRT-PCR) was used to measure RNA levels of selected centromere genes identified by RNA sequencing. Actin mRNA was used as the internal control. I The indicated ovarian cancer cell lines were treated with vehicle or 5 µM BAY-850 for 48 h, and centromere protein E (CENPE) protein levels were measured via immunoblotting. ACTINB was used as loading control. Data represent the mean ± standard error for three biological replicates. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns: not significant.

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