الفهرس 
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Abstract
Cancers of the colon and rectum are among the most common and deadly neoplasms. Up to half of CRC patients develop local recurrence and distant metastasis which represent a major hurdle in the treatment of this cancer. Therefore, exploring the underlying mechanisms involved in CRC metastasis and progression is aiming to develop new therapeutic strategies for CRC patients. Epithelial-mesenchymal transition has been proposed as a critical mechanism during cancer progression that endows cancer cells with increased motility and invasiveness to seed metastasis. Thus, EMT pathways are of increasing interest as a novel therapeutic avenue in the treatment of cancer that could be targeted to prevent tumor cell dissemination in early stage patients. The EMT is tightly regulated by several internal and external cues that orchestrate the shifting from tightly-interacting and immotile epithelial-like phenotype into loosely-adherent and motile mesenchymal phenotype, to promote metastatic development. During the EMT, the expression of epithelial markers is down-regulated, while the expression of mesenchymal markers is up-regulated. Several oncogenic pathways have been reported to induce EMT. These signaling pathways crosstalk to each other and converge to key transcription factors to turn on the core switches of EMT, initialize and maintain the process of EMT. Importantly, both the TGF-β pathway and other signaling cascades including Wnt, often cooperatively, induce EMT during cancer