biostudies-literatureSun DLiaoning Provincial Eduication FoundationLiaoning Provincial Natural Science Foundatione0274919https://www.ebi.ac.uk/biostudies/studies/S-EPMC9498949biostudies-literatureUnknown17(9)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.PloS oneMicroRNA-206 suppresses growth and metastasis of breast cancer stem cells via blocking EVI-1-mediated CALR expression.PMC9498949JYTCZR2020051201805506012019-ZD-0833Zhang FLi CSun DfalseMicroRNA-206 suppresses growth and metastasis of breast cancer stem cells via blocking EVI-1-mediated CALR expression.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.2022-01-01T00:00:00Z20222025-04-18T20:52:13.881Z2025-04-07T08:52:20.359ZS-EPMC94989493613697210.1371/journal.pone.0274919