Abstract
Aim to investigate the effect of miR-206 on the growth and metastasis of breast cancer stem cells and clarify the precise mechanism of miR-206 on EVI-1-mediated CALR expression in driving malignant phenotype. Our results showed that miR-206 mimics suppressed CALR expression, inhibited the proliferation and metastasis ability of breast cancer stem cells and finally induced cellular apoptosis. Over-expression of CALR could effectively attenuate the cytotoxic effect of miR-206. Further studies demonstrated that EVI-1 could be served as a key regulator of miR206-mediated CALR expression. Elevation of EVI-1 can reverse the function of miR-206 on induction of CALR.