EMT (Epitheliomesenchymal transition) is a process where tumor cells attain mesenchymal features which make it easier for them to invade and metastasize [94, 95] . It is regulated by transcription factors such as snail, slug, twist and zeb1 [94] [95] [96] . In mouse mammary epithelial cells snail induced EMT and at the same time [97] . In lung carcinoma there was an inverse association between zeb1 and claudins 1 and 2 and between twist and claudin 5 [63] . Metastatic tumors to the lung also showed an inverse association between claudins 5 and 7 and twist [63] . These results show that a part of claudin expression is regulated by EMT associated transcription factors and that claudins are involved in EMT. Also different PKCs which regulate claudin phosphorylation are overexpressed in cancer and may cause dysregulation or relocation of claudins in tumor cells [98] . PKCε is considered an oncogene and influences cellular motility and ras expression, and it is upregulated in lung and breast cancer [98] . PKC and PKA influence subcellular distribution of claudin 1 in melanoma cells [99] . PKCα phosphorylates claudin 5 causing its disappearance from cell membrane [100] . On the other hand, phosphorylation of serine 194 of claudin 4 by aPKC is required for tight junction formation in keratinocytes [101] . Claudin phosphorylation may also affect barrier junction permeability without changes in claudin distribution [101] .