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. Author manuscript; available in PMC: 2019 Mar 27.
Published in final edited form as: Cancer Res. 2017 Dec 19;78(5):1225–1240. doi: 10.1158/0008-5472.CAN-17-1089

Figure 3. The CBM signalosome mediates NF-κB activation and gene expression reprogramming in AGTR1+ breast cancer.

Figure 3.

A, effect of siRNA-mediated knockdown of each individual component of the CBM signalosome on Ang II-dependent NF-κB activation in either BT549 or ZR75-AGTR1 cells. B, effect of losartan (5 µM) or IKK-VI (5 µM) on Ang II-dependent NF-κB activation in AGTR1+ breast cancer lines. As expected, the response to TNFα is blocked only by IKK-VI and not losartan. C, siRNA-mediated Bcl0 knockdown in BT549 cells and effect on NF-κB gene targets. D, heatmap of gene expression changes in BT549 cells following Bcl10 knockdown by siRNA, in biological triplicate (upregulated=red, downregulated=blue). Analysis includes 487 genes from the Nanostring Pancancer Progression codeset for which expression could be reliably determined. E, Ingenuity Pathway Analysis (IPA) based on data from panel (D). Bar graphs indicate level of significance of change in the indicated pathways (-log p value). Increasingly dark blue color indicates greater reduction in pathway activity, while increasingly dark orange color indicates greater enhancement.