A key stone of cancer invasion is the disruption of the cellular junctions through the Diacerein downregulation of the function and/or important signaling pathways carried out by critical cell adhesion molecules such as cadherins and integrins. This loss of adhesiveness allows tumor cells to disobey the social order, resulting in the alteration of the normal histological structure and dissociation from cancer nests. In particular, adherens junctions, which are orchestrated by Ecadherin molecule, provide adhesive contacts between neighboring epithelial cells and form intracellular interactions to the actin cytoskeleton, being involved in important signaling processes leading to the regulation of gene transcription. It is not surprising that in most, if not all, cancers of epithelial origin Ecadherin-mediated cell-cell adhesion is downregulated or inactivated promoting cancer cell invasion and metastases. In addition, E-cadherin is one of the key molecular markers along the process of Epithelial to Mesenchymal Transition, which is a BRL-54443 fundamental biological process associated with the progression from adenoma to carcinoma and the subsequent steps of cancer cell invasion and metastasis. Integrins are transmembrane receptors that bind to ECM components and are involved in adhesion and migration processes. They are composed of a and b heterodimers, lack endogenous enzymatic activity and depend on signal transducers to perform their functions, such as the nonreceptor focal adhesion kinase as well as a variety of scaffolding proteins that link integrins to the actin cytoskeleton. As a result of cell adhesion to ECM components, integrins transmit information that regulates intracellular signaling. Specifically, FAK is activated via autophosphorylation at tyrosine 397 upon integrin binding to its ligands. Phosphorylated FAK Y397 becomes a binding site for the tyrosine kinase Src, and FAK/Src complex then activates other downstream proteins, e.g. pCAS, Crk or paxillin, which in turn activate important pathways involved in cell migration progress.