Epithelial Mesenchymal Transition (EMT) is an event where epithelial cells acquire mesenchymal-
like phenotype. EMT can occur as a physiological phenomenon during tissue development and
wound healing, but most importantly, EMT can confer highly invasive properties to epithelial carcinoma
cells. The impairment of E-cadherin expression, an essential cell-cell adhesion protein, together
with an increase in the expression of mesenchymal markers, such as N-cadherin, vimentin, and fibronectin,
characterize the EMT process and are usually correlated with tumor migration, and metastization.
A wide range of micro-environmental and intracellular factors regulate tumor development and progression. The
dynamic cross-talk between the adhesion-related proteins such as E-cadherin and the EMT-related transcription factors,
with special focus on TWIST, will be discussed here, with the aim of finding a suitable biological pathway to be used as
potential target for cancer therapy. Emerging concepts such as the role of the PI3K/AKT/TWIST pathway in the regulation
of the E-cadherin expression will be highlighted, since it seems to be consistently involved in cells EMT. The wellknown
efficacy of the RNA interference as a tool to silence the expression of specific proteins has come into focus as a
strategy to control different tumor sub-populations. Despite the oligonucleotides enormous sensitivity and low in vivo stability,
new (nano)technological solutions are expected to enable RNAi clinical application in cancer therapy.