ABSTRACT
Breast cancer progression depends on host innate and adaptive immune responses. Despite the effect of immune system in tumor destruction, cancer cells may induce the immune cells to support tumor progression. During tumor-host interactions, both tumor and immune cells produce signicant amounts of reactive species (RS). The imbalance resulting from RS production and its neutralization is called oxidative stress, and it modulates several cellular processes impacting breast cancer outcome. Two major sensors of these processes are the nuclear factor erythroid-derived 2-related factor 2 (NRF2) and NF-κB-related pathways. The transcriptional factor NF-κB has prooxidant capacity, while Nrf2 has neutralizing action. NF-κB is a regulator of innate immunity, and it induces RS production and inammatory cytokines. Furthermore, high level of NF-κB is found for breast cancer, and its downstream signaling has been implicated in aggressive tumor features. The redox sensor NRF2 is activated under oxidative stress conditions and induces human antioxidant response element in order to control cellular homeostasis; however, it protects tumors against RS caused by chemotherapy leading to treatment resistance. This chapter raises the discussion regarding the redox mechanisms involved in breast cancer development driven by the activation of the Nrf2-NF-κB axis.
