Fig. 5

Model displaying the association of ANP32E expression levels with multiple characteristics of breast cancer. In Basal-L tumors, arising from a multipotent progenitor, we find that ANP32E may 'lock-in' a pattern of accessible chromatin favoring SOX9 binding, proliferation and self-renewal. Alternatively, in HR+ breast tumors arising from a more differentiated luminal progenitor, ANP32E restricts FOXA1 binding such that luminal identify and hormone responsiveness is maintained. The loss of ANP32E may therefore increase FOXA1 binding, relax cellular programming and increase the metastatic potential of the tumor