The disseminate from primary tumor sites by using either

The occurrence of invasion and metastasis is the major cause for most cancer-related deaths. During metastatic
progression of carcinoma, polarized epithelial tumor cells gain invasive and migratory characteristics, leave the
primary site, invade the basement membrane beneath, intravasate into blood or lymph vessels, transport through
the circulation, extravasate from the circulation, disseminate into the secondary site, and grow at the metastatic
foci. Epithelial carcinoma cells disseminate from primary tumor sites by using either collective cell migration
(2) or single cell migration such as round shape, non-proteolytic amoeboid migration (3) and mesenchymal-type
movement (4). This phenotypic conversion enables tumor cells dissociate from their original tissue and form
metastasis in distant organ. This epithelial cell plasticity caused by breakdown of epithelial cell homeostasis
leading to malignant cancer progression has been associated with the loss of epithelial traits and the acquisition
of migratory phenotype. In carcinomas,cells awakening the event of mesenchymal transition become motile and
increase invasive ability (4). Hence, the phenotypic transition from epithelial to mesenchymal-like cell state
represents one important mechanism for epithelial plasticity and cancer metastasis.
Recent studies have implicated the role of Twist, the basic helix–loop–helix transcription factor in the early
steps of metastasis (5,6). Twist has been previously known to be involved in neural crest cell migration and
mesoderm differentiationand has recently been identified for genes associated with metastasis to the lungs of
murine mammary tumor lines. Moreover, studies demonstrate that Twist overexpression results in EMT of
human immortalized mammary epithelial cells, which is characterized by downregulation of E-cadherin, betaand
italic gamma-catenin, upregulation of fibronectin and vimentin, spindle-like morphological changes and
increased migratio