Figure 1.

E-cadherin mediates micrometastatic dormancy and chemoresistance. Hepatocytes induce E-cadherin upregulation in metastatic prostate cancer as well as other epithelial markers, thus promoting a partial cancer-associated mesenchymal-to-epithelial reverting transition (cMErT) by initial suppression of p38 and ERK. Upon cell-cell E-cadherin ligandation, stimulation of metastatic cells with chemotherapy induces activation of canonical pro-survival kinases resulting in increased chemoresistance. This chemoresistance is proliferation-independent and can be targeted with an adjuvant treatment to achieve optimal efficacy with traditional chemotherapies. DTCs: disseminated tumor cells.