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. Author manuscript; available in PMC: 2015 Nov 1.
Published in final edited form as: Biochim Biophys Acta. 2014 Jul 30;1843(11):2620–2630. doi: 10.1016/j.bbamcr.2014.07.012

Fig. 3.

Fig. 3

Suppression of Bcl3 inhibits expression of anti-apoptotic genes, but induces expression of pro-inflammatory genes in CTCL cells. (A) Real time RT-PCR analysis of cIAP1, cIAP2, Bcl2, IL-8 and IL-17 mRNA levels in Hut-78 cells transfected with control non-silencing siRNA or shRNA (full columns), and Bcl3 specific siRNA (empty columns) or shRNA (gray columns). The values represent the mean ± SE of four experiments. Asterisks denote a statistically significant (p < 0.05) change compared to cells transfected with the corresponding control RNA. (B) Western analysis of total protein levels of Bcl3, cIAP1, cIAP2, Bcl2, and control actin, in Hut-78 cells transfected with control non-silencing and Bcl3 specific siRNA or shRNA. (C) Densitometric evaluation of cIAP1, cIAP2 and Bcl2 densities shown in panel B. The cIAP1, cIAP2 and Bcl2 protein/actin values in cells transfected with control RNA were arbitrarily set to 100%, and the protein/actin values in cells transfected with Bcl3 siRNA or shRNA are presented relative to those values. The data represent the mean of four experiments ± SE, and the asterisks denote a statistically significant (p < 0.05) change compared to cells transfected with the corresponding controls. (D) IL-8 and IL-17 release measured by ELISA in cell culture supernatants of Hut-78 cells transfected with control non-silencing siRNA or shRNA (full columns) and Bcl3 specific siRNA (empty columns) or shRNA (gray columns). The values represent the mean ± SE of four experiments. Asterisks denote a statistically significant (p < 0.05) change compared to cells transfected with the corresponding controls.

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