Fig. 2: XIAP overexpression is mediated through NF-kB dependent mechanisms. | British Journal of Cancer

Fig. 2: XIAP overexpression is mediated through NF-kB dependent mechanisms.

From: BRCA mutations lead to XIAP overexpression and sensitise ovarian cancer to inhibitor of apoptosis (IAP) family inhibitors

Fig. 2

a NF-kB p65 interacts with the promoter of XIAP in both the BRCA1-mutated UWB1289 and the isogenic UWB1289-BRCA1 cell lines (n = 2). b, d, e The level of phosphorylation of NF-kB –p65 at S536, NF-kB –p50 and NF-kB –p105, evaluated by western blot, were higher in the BRCA1-mutated ovarian cancer (OC CL) UWB1289 compared with the isogenic BRCA1-restored OC CL UWB1289-BRCA1 (n = 3). c The level of expression of NF-kB -p65 is similar in the UWB1289 and UWB1289-BRCA1 (n = 3). f Treatment with 5 µM BMS-345541 for 24 h decreased levels of XIAP mRNA in UWB1289 (BRCA1-MUT) and UWB1289-BRCA1 (BRCA1-restored) (n = 3). XIAP mRNA intensity is shown as a percentage of that in untreated UWB1289 after normalisation with the level of expression of GAPDH mRNA in the corresponding CLs. g Treatment with 5 µM of the inhibitor of NF-Kb pathway BMS-345541 for 24 h led to a decrease of XIAP protein expression only in the BRCA1-mutated OC CL UWB1289 (n = 3).

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