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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Oncogene. 2014 Sep 15;34(28):3700–3710. doi: 10.1038/onc.2014.302

Figure 3. Blocking of NF-κB signaling increases the sensitivity of androgen-independent PCa cells to the anti-androgen.

Figure 3

C4-2B cells were stably infected with IKK2-KD retroviral vector (C4-2B-KD), in which NF-κB activity was inhibited with a kinase dead (KD) IKK2 mutant. The cells infected with empty vector (EV) were used as controls leaving NF-κB signaling activated (C4-2B-EV). Both A) C4-2B-EV and B) C4-2B-KD cells were treated with Bicalutamide (Bic). Cell proliferation assay was performed at 48 hours after treatment. Results are presented as means ± SD of 3 experiments performed in triplicate. C) NF-κB signaling activated (LNCaP-EE) and inactivated (LNCaP-EV) LNCaP cells were treated with or without androgen (DHT; 10−8M). Cell proliferation assay was performed at 72 hours after treatment. Results are presented as means ± SD of 3 experiments performed in triplicate. **, P < 0.001 by Student’s t test.