Abstract

Epithelial-mesenchymal transition (EMT) is an important process during development by which epithelial cellsb acquire mesenchymal, fibroblastlike properties and show reduced intercellular adhesion and increased motility.The identification of epithelial-mesenchymal plasticity of breast cancer stem cells provided another level of complexity regarding development of strategies to eliminate these lethal seeds of breast cancer. In determining the association between Sox2, cell migration and expression of EMT markers, we found a persistently high expression of Twist1 and its apparent lack of EMT-like properties during migratory arrest of MDA-MB-231 cells, even after paclitaxel treatment of Sox2-silenced cells. The role of Sox2-dependent Twist1 in maintaining stemness was more prominent when Sox2 expression was high in brCSCs. It can be presumed now that Twist1 expression in presence or absence of Sox2 defines the precise mechanism underlying the possible role of Twist1 in crossroads of pluripotency and EMT of breast cancer stem cells.

Keywords: Breast cancer; Breast cancer stem cells; Pluripotency;Epithelial-to-mesenchymal transition;Chemoresistance; SOX2; Chemotherapy; TWIST1; ABCG2;Gene silencing