Dormant DCC immune evasion and activation to form metastasis.

This simplified model shows that microenvironmental cues, such as TSP-1, induce and maintain dormancy. Dormant DCCs down-regulate E-cadherin expression and up- regulate UPR activity, which results in MHC-I down-regulation and immune evasion from CD8+ T cells. Eventually, unpredictable changes in the host cause inflammation and other tissue-wide changes. Inflammation can recruit neutrophils to produce NETs and the associated proteases cause proteolytic processing of laminin-111 and TSP1 degradation. This causes α3β1 integ sin-mediated activation of dormant DCCs that proliferate to form metastasis.