The conserved polarity proteins Par6 and aPKC regulate cell polarization 
processes. However, increasing evidence also suggests that they play a role in 
oncogenic progression. During tumor progression, epithelial to mesenchymal 
transition (EMT) delineates an evolutionary conserved process that converts 
stationary epithelial cells into mesenchymal cells, which have an acquired 
ability for independent migration and invasion. In addition to signaling 
pathways that alter genetic programes that trigger the loss of cell-cell 
adhesion, alternative pathways can alter cell plasticity to regulate cell-cell 
cohesion and increase invasive potential. One such pathway involves TGFβ-induced 
phosphorylation of Par6. In epithelial cells, Par6 phosphorylation results in 
the dissolution of junctional complexes, cytoskeletal remodelling, and increased 
metastatic potential. Recently, we found that aPKC can also phosphorylate Par6 
to drive EMT and increase the migratory potential of non-small cell lung cancer 
cells. This result has implications with respect to homeostatic and 
developmental processes involving polarization, and also with respect to cancer 
progression-particularly since aPKC has been reported to be an oncogenic 
regulator in various tumor cells.