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The metastatic process involves the migration and invasion of cancer cellsthroughout the body to produce secondary tumors at distant sites. Through of epithelial-mesenchymaltransition (EMT), cancer cells employ developmental processes to gain migratoryand invasive properties. CD44 is the transmembrane adhesion receptor for Hyaluronan(HA) and plays a central role in the remodeling and degradation of HA that leadsto cell migration, as well as to cancer invasion and metastasis. CD44 is highlyexpressed in primary and metastatic colon cancer but lowly expressed in normaltissues. We evaluated the impact of CD44 on EMT and invasion of colon cancer cells.The functional role of CD44 in EMT was determined by the overexpression or knockdownof CD44. CD44 was overexpressed by transfection with plasmid-RT-PCR product andknockdown of CD44 by small hairpin RNA (shRNA)-mediated depletion of CD44 in SW480colon cancer cells. Morphological changes were evaluated by confocal laser microscopyin the culture media. The expression of EMT markers (E-cadherin/N-cadherin/vimentin/fibronectin/actin/MMPs)and CD44/EGFR/PI3K-Akt signaling were evaluated using western blotting. The influenceof EMT in tumor biology was assessed with proliferation, migration and invasionassays. EMT changes increased in CD44-overexpressing SW480 cells and decreasedin CD44 knockdown cells. CD44 activation induced expression of EGFR and activationof phosphatidylinositol 3' kinase (PI3K)/Akt and expression of glycogen synthasekinase-3 β (GSK-3β). In terms of EMT markers, CD44 downregulated E-cadherin expression,upregulated N-cadherin, α-actin, vimentin, fibronectin and MT1-MMP, and inhibitedthe formation of the membrane-associated E-cadherin-β-catenin complex, which resultedin cell invasion and migration.

CD44 enhances the epithelial-mesenchymal transition in association with colon cancer invasion