PIPK1b regulates E-cadherin endocytosis in polarized breast cancer cells and promotes a switch to a migratory phenotype

Abstract

The endocytosis, degradation, and recycling of cadherins is crucial for the dynamic regulation of adherens junctions and the control of cell-cell adhesion during tissue formation and in many pathological conditions. In order to allow for dynamic changes in intercellular adhesion, adherens junctions assemble and disassemble in a continuous fashion. A key mechanism for modulating adhesion strength is the adjustment of the cell surface levels of E-cadherin, the major component of adherens junctions. E-cadherin endocytosis, often accompanied by its degradation, has been observed in many developmental and disease processes and accounts for more rapid changes in adhesion strength that can occur independently of the transcriptional regulation of E-cadherin. However, the molecular mechanisms underlying E-cadherin endocytosis and recycling remain incompletely understood.