fig7

Figure 7. MUC1-C drives the progression of wound repair to cancer. In response to the loss of homeostasis, MUC1-C activates inflammatory STAT3 and NF-κB pathways that induce EMT, stemness, and methylation of DNA and histones. These pathways are integrated with activation of E2F and MYC in driving reversible proliferative and chromatin remodeling pathways associated with the resident SC inflammatory memory response. In settings of chronic inflammation, prolonged MUC1-C activation irreversibly establishes this memory response and drives the CSC state with drug resistance, immune evasion, genomic instability, and poor clinical outcomes. EMT: Epithelial-mesenchymal transition; SC: stem cells; CSC: cancer stem cell.