Skip to main content
. 2014 Dec 29;9(4):791–805. doi: 10.1016/j.molonc.2014.12.007

Figure 3.

Figure 3

Increased CXADR transcript levels results from histone modification; increased expression in paclitaxel‐resistant ovarian cancer in mice and humans. A. ChIP was performed with sheared chromatin with antibodies against H3K4me3 or H3K27ac. Percentage input was calculated as per Supplementary Methods. B. SKOV3 and A2780 cells were treated with 30–300 nM TSA for 24 h. CXADR transcript number was assessed by qRT‐PCR. ***; p < 0.001. C. SKOV3 and A2780 cells were also treated with 30 nM paclitaxel or 300 nM nocodazole for 24 h to induce G2/M arrest. CXADR transcription was assessed by qRT‐PCR. D. Female ICRF nu/nu mice bearing intraperitoneal SKOV3 xenografts were treated with weekly intraperitoneal PBS or paclitaxel (10 mg/kg). **; p < 0.01. E. CXADR transcript level was quantified in tumours excised from PBS‐ and paclitaxel‐treated mice, relative to 18S. ***; p < 0.001. F. Expression of CAR was assessed by IHC in 5 μm sections. Bars represent 50 μm. G. Expression of CAR in duplicate cores from archival tumour samples from patients in the SaPPrOC trial of weekly paclitaxel chemotherapy was assessed and correlated against best clinical response. *; p < 0.05. H. CXADR transcription in tumours samples from CTCR OV01 trial was correlated with best clinical outcome.