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Figure 4 | Molecular Cancer

Figure 4

From: Retinoic acid protects human breast cancer cells against etoposide-induced apoptosis by NF-kappaB-dependent but cIAP2-independent mechanisms

Figure 4

9-cis-RA treatment results in in vivo recruitment of p65 and retinoic-acid receptors, RAR and RXR to the cIAP2 promoter. (A) EMSA performed with probes bearing the NF-κB-1 and NF-κB-3 sites of the cIAP2 promoter and nuclear extracts from T47D cells treated with 1 μM 9-cis-RA for 1 h. When indicated, antibodies directed against p65 were present in the binding assays. The images shown are from one representative experiment performed twice with similar results. B) T47D breast cancer cells were treated as indicated in Material and Methods and ChIPs assays were performed using antibodies against p65, RARs, RXRα, cJUN or acetyl-H3 histone. Immunoprecipitated chromatin was analyzed by real time PCR using primers specific for the cIAP2, RARβ2 and cJUN promoters. Shown are data from a representative experiment, expressed as fold induction relative to the values obtained with immunoglobulin G (IgG) used as a negative control, which were set to 1. This experiment was repeated three times with similar results.

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