fig4

Figure 4. Crosstalk regulation of Nrf-2, NF-κB and AR signaling in CRPC cells. Hormone deprivation (ADT) induced oxidative stress and redox signaling activates both NF-κB and AR signaling that facilitates CRPC progression. Oxidative stress also increases Nrf2 nuclear levels which blocks both NF-κB and AR signaling. Thus, reduction of oxidative stress post-ADT by using potent Nrf2-activating agents may prevent CRPC outgrowth. CRPC: castrate resistant prostate cancer; NF-κB: nuclear factor kappa B; AR: androgen receptor