RESEARCH Oncogenic transformation cells decreases Nrf2 expre r

Full list of author information is available at the end of the articleBackground An increase in reactive oxygen species (ROS) is a com-mon biochemical property of cancer cells [1,2]. However, excess ROS also induce senescence, cell cycle arrest and apoptosis [3], indicating that redox homeostasis is tightly regulated in tumor cells. To offset excess ROS cells have developed regulatory mechanisms, including the induc-tion of antioxidant enzymes and/or the activation of redox buffering systems such as glutathione. The tran-scription factor Nrf2 (NFE2L2) plays a crucial role in the cellular defense against oxidative stress through its abi-lity to induce the expression of antioxidant and deto-xification genes [4,5]. Under basal conditions, Nrf2 is bound to its inhibitor Keap1 and targeted for degra-dation by the proteasome pathway [6,7]. Upon certain stress conditions, Nrf2 is released from the inhibitory complex and translocates to the nucleus where it bind