Abstract
Nuclear factor E2-related factor 2 (Nrf2) is a redox-sensitive transcription factor regulating the expression of a battery of genes encoding antioxidant and carcinogen detoxifying enzymes. In contrast to its tumor suppressive functions in normal cells, Nrf2 facilitates tumor growth and progression through metabolic reprograming in some cancer cells. Our previous study has demonstrated that 15-deoxy-Δ12,14-prostaglandin J2 and 4-hydroxyestradiol induce overactivation of Nrf2 and consequently overexpression of its target protein, heme oxygenase-1 (HO-1), in human breast cancer cells. More recently, we have demonstrated the involvement of Nrf2 in experimentally induced hepatocarcinogenesis (N.H.K. Chi et al., Cancer Res., 2017). In this context, the cellular stress response or cytoprotective signaling mediated via the Nrf2-HO-1 axis is hijacked by cancer cells. This may facilitate the remodeling of the tumor microenvironment making it advantageous for the autonomic growth of cancer cells, metastasis, angiogenesis, tolerance to anticancer therapy, and self-renewal activity of stem-like cells.
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