Adhesion is an essential process to epithelial cells so that epithelium can be formed and cells can be in permanent contact with extracellular matrix and other cells. Several pathways exist to accomplish this communication and adhesion with environment. But the main signalling pathways are the cadherin and integrin pathways.
The cadherin pathway is present in adhesion junctions or in desmosomes and it is responsible for epithelial adhesion and communication with adjacent cells. Cadherin is a transmembrane glycoprotein receptor that establishes contact with another cadherin present in the surface of a neighbour cell forming an adhesion complex. This adhesion complex is formed by β-catenin and α-catenin, and p120 is essential for its stabilization and regulation. This complex then binds to actin, leading to polymerization. For actin polymerization through the cadherin pathway, proteins of the Rho GTPases family are also involved. This complex is regulated by phosphorylation, which leads to downregulation of adhesion. Several factors can induce the phosphorylation, like EGF, HGF or v-Src. The cadherin pathway also has an important function in survival and proliferation because it regulates the concentration of cytoplasmic β-catenin. When β-catenin is free in the cytoplasm, normally it is degraded, however if the Wnt signalling is activated, β-catenin degradation is inhibited and it is translocated to the nucleus where it forms a complex with transcription factors. This leads to activation of genes responsible for cell proliferation and survival. So the cadherin-catenin complex is essential for cell fate regulation. 
Integrins are heterodimeric glycoprotein receptors that recognize proteins present in the extracellular matrix, like fibronectin and laminin. In order to function, integrins have to form complexes with ILK and Fak proteins.  For adhesion to the extracellular matrix, ILK activate the Rac and Cdc42 proteins and leading to actin polymerization. ERK also leads to actin polymerization through activation of cPLA2. Recruitment of FAK by integrin leads to Akt activation and this inhibits pro-apoptotic factors like BAD and Bax. When adhesion through integrins do not occur the pro-apoptotic factors are not inhibited and resulting in apoptosis.