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. Author manuscript; available in PMC: 2011 Mar 9.

Published in final edited form as: Int J Cancer. 2009 Aug 1;125(3):565–576. doi: 10.1002/ijc.24271

[a] Evaluation of NF-κB family members, NF-κB1 (p50) and RelA (p65) in tumor sections from mice treated with CAPE (10 mg/Kg BW with 0.1% DMSO) or vehicle (1:1/DMSO: NaCl). Immunohistochemical analysis shows that both NF-κB1 (p50) and RelA (p65) are downregulated after CAPE treatment compared to vehicle. Orig. magnification × 20. [b] Immunoblotting analysis for NF-κB1 (p50) and RelA (p65) in tumor sections from from mice treated with CAPE (10 mg/Kg BW with 0.1% DMSO) or vehicle (1:1/DMSO: NaCl). Protein expression was downregulated for both p50 and p65 in CAPE- treated mice samples compared to vehicle. Alpha-tubulin levels were unchanged in vehicle- and CAPE- treated tumor samples.

Data are ± SEM of 4 experiments. *p< 0.05 compared to basal (0.1% DMSO).

[a] Evaluation of NF-κB family members, NF-κB1 (p50) and RelA (p65) in tumor sections from mice treated with CAPE (10 mg/Kg BW with 0.1% DMSO) or vehicle (1:1/DMSO: NaCl). Immunohistochemical analysis shows that both NF-κB1 (p50) and RelA (p65) are downregulated after CAPE treatment compared to vehicle. Orig. magnification × 20. [b] Immunoblotting analysis for NF-κB1 (p50) and RelA (p65) in tumor sections from from mice treated with CAPE (10 mg/Kg BW with 0.1% DMSO) or vehicle (1:1/DMSO: NaCl). Protein expression was downregulated for both p50 and p65 in CAPE- treated mice samples compared to vehicle. Alpha-tubulin levels were unchanged in vehicle- and CAPE- treated tumor samples.

Data are ± SEM of 4 experiments. *p< 0.05 compared to basal (0.1% DMSO).