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Introduction   MYB  is highly expressed in estrogen receptor positive (ER + ve) breast tumours and tumour cell lines. We recently demonstrated that  MYB  is essential for the proliferation of ER + ve breast cancer cells, and have now investigated its role in mammary epithelial differentiation.    Methods  MCF-7 breast cancer cells were treated with sodium butyrate, vitamin E succinate or 12-O-tetradecanoylphorbol-13-acetate to induce differentiation as measured by Nile Red staining of lipid droplets and β-casein expression. The non-tumorigenic murine mammary epithelial cell (MEC) line, HC11, was induced to differentiate with lactogenic hormones.  MYB  levels were manipulated by inducible lentiviral shRNA-mediated knockdown and retroviral overexpression.    Results  We found that  MYB  expression decreases following chemically-induced differentiation of the human breast cancer cell line MCF-7, and hormonally-induced differentiation of a non-tumorigenic murine mammary epithelial cell (MEC) line, HC11. We also found that shRNA-mediated  MYB  knockdown initiated differentiation of breast cancer cells, and greatly sensitised them to the differentiative and pro-apoptotic effects of differentiation-inducing agents (DIAs). Sensitisation to the pro-apoptotic effects DIAs is mediated by decreased expression of  BCL2 , which we show here is a direct  MYB  target in breast cancer cells. Conversely, enforced expression of  MYB  resulted in the cells remaining in an undifferentiated state, with concomitant suppression of apoptosis, in the presence of DIAs.    Conclusions  Taken together, these data imply that  MYB  function is critical in regulating the balance between proliferation, differentiation, and apoptosis in MECs. Moreover, our findings suggest  MYB  may be a viable therapeutic target in breast cancer and suggest specific approaches for exploiting this possibility.

MYBsuppresses differentiation and apoptosis of human breast cancer cells