Breast cancer occurs at a high frequency in women and, given this fact, a primary focus of breast cancer research has been the study of estrogen receptor signaling. However, androgens are known to play a role in some normal breast physiology and therefore androgen receptor signaling also may be important in breast carcinogenesis. Moreover, the presence of androgen receptor in breast cancer makes it an attractive therapeutic target but the ability to exploit androgen receptor for therapy has been difficult. This is in part because androgens can either inhibit or stimulate cell proliferation in preclinical models of breast cancer. In addition, many breast cancers co-express other steroid hormone receptors such as estrogen receptor and progesterone receptor which can affect androgen receptor signaling and obfuscate the effects of androgens. To elucidate the role of androgens, the work presented here reports the generation of both malignant and benign estrogen and progesterone receptor negative human breast epithelial cell lines engineered to express androgen receptor. Experiments using these models show that concurrent hyperactivation of the mitogen activated protein (MAP) kinase pathway from androgen receptor and extracellular growth factor signaling results in an anti-proliferative response whereas MAP kinase signaling from either androgen receptor or extracellular growth factor signaling alone results in cellular proliferation. Additionally, in the benign cell line, gene knockdown and gene knockout studies demonstrate that activation of the MAP kinase pathway via androgen receptor signaling is dependent on p21. These findings provide a mechanistic explanation for previous observations ascribing a dual role for androgen receptor in breast cancer cells, and provide new insights for exploiting androgen receptor as a target for breast cancer therapy.