SLUG, a member of the SNAIL family of transcriptional repressors, is known to play a diverse number of roles in the cell, and its deregulation has been observed in a variety of cancers including breast. Here, we focus on SLUG's role as a master regulator of mammary epithelial cell (MEC) fate and lineage commitment in the normal mammary gland, and discuss how aberrant SLUG expression can influence breast tumor formation, phenotype, and progression. Specifically, we discuss SLUG's involvement in MEC differentiation, stemness, cellular plasticity, and the epithelial to mesenchymal transition (EMT), and highlight the complex connection between these programs during development and disease progression. Undoubtedly, delineating how molecular factors influence lineage identity and cell-state dynamics in the normal mammary gland will contribute to our understanding of breast tumor heterogeneity.
Keywords: BCSC, Breast Cancer Stem Cell; BM, Basement Membrane; BRCA1, Breast Cancer Associated 1; CK, Cytokeratin; CSC, Cancer Stem Cell; E-CAD, E-Cadherin; EMT; EMT, Epithelial to Mesenchymal Transition; ERα, Estrogen Receptor; HDAC, Histone Deacetylasae; HMECs, Human Mammary Epithelial Cells; IHC, Immunohistochemical; LSD1, Lysine Specific Demethylase 1.; ME, Myoepithelial; MEC, Mammary Epithelial Cell; MaSC, Mammary Stem Cell; SLUG; SMA, Smooth Muscle Actin; SNAG, Snai.Gfi-1; WT, Wild type; breast cancer; cellular plasticity; differentiation; mammary stem cells.