Fig. 8
From: The effect of Nrf2 deletion on the proteomic signature in a human colorectal cancer cell line
Overview of pathways elucidated by our research in HT29-Nrf2− cells. In the absence of Nrf2, oxidative condition can activate several cell survival and stress response pathways. Based on our proteomic date, an increase in p38 and JNK and their upstream proteins could elevate the expression of FOXO3/4. FOXO protein translocation to the nucleus enhances SOD2 expression. In addition, FOXO protein can affect mitochondrial gene expression. Enhancement of Raf expression rise its downstream ERK 1/2 expression. Both ERK 1/2 and FOXO3/4 induces a specific set of genes involved in the regulation of various cellular processes. Also noncanonical Notch pathways may be activated by an increase in ROS and expression of 𝛾-secretase and ADAM 17 . Noncanonical Notch signaling interacts with MAPKs signaling and other pathways that could affect proliferation and EMT process