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EVL belongs to the Ena/VASP (Enabled/vasodilator-stimulated phosphoprotein) family of proteins [Mena (mammalian Ena), VASP and EVL], which have a range of roles in regulating the actin cytoskeleton. Growing evidence suggests that Mena and VASP are involved in carcinogenesis, though little is known about the significance of EVL's function in cancer. This study examined the expression levels of EVL mRNA in paired breast cancer specimens using semi-quantitative and real-time RT-PCR. In a comparison between matched breast tumors and normal tissues, a significant increase in the level of EVL mRNA was found in 23 of the 35 (65.7%) tumors (P=0.032). Patients in the advanced stages more frequently exhibited an elevated EVL expression in tumor tissues. The EVL mRNA relative expression level significantly correlated with clinical stages (P=0.021). To begin elucidating the mechanism, we measured the ability of EVL to transform NIH3T3 cells and regulate the motility of MCF-7 cells in vitro by focus formation and modified Boyden chamber assays. The results indicated that overexpression of EVL was insufficient to transform NIH3T3 cells, although the motility of EVL transfected MCF-7 cells was markedly promoted. Collectively, EVL expression level was higher in breast tumors compared to normal tissues and its up-regulation was positively associated with the clinical stages of breast cancer. Additionally, EVL may be implicated in invasion and/or metastasis of human breast cancer.

EVL (Ena/VASP-like) expression is up-regulated in human breast cancer and its relative expression level is correlated with clinical stages