Breast cancer patients who suffer from a relapse and develop metastatic disease are currently incurable due to the lack of targeted therapies, especially in patients diagnosed with triple-negative breast cancer (TNBC) subtype. MicroRNAs (miRNAs) are now regarded as potent regulators of a myriad of cellular processes in development and in oncogenesis. We are interested in identifying miRNAs that are critical in regulating mammary ductal development, cancer progression and metastasis by utilising an ex vivo developmental model, the terminal end buds (TEBs) in pubertal mice. TEBs are poorly differentiated, highly proliferative, invasive, and enriched for stem and progenitor cell activity, which recapitulate certain hallmarks of cancer in a tightly controlled manner. miRNA expression profiling on the TEBs and mature ducts has identified a subset of candidate miRNAs that might be crucial during mammary gland development. miR-184 was the most highly enriched miRNA in the mature ducts. Further examination of miR-184 showed that it is silenced in a panel of breast cancer cell lines and some mouse tumour models. Functional characterisation of miR-184 in cancer revealed that miR-184 overexpression inhibits proliferation, self-renewal in metastatic TNBC cells; it delays tumour formation and distant metastatic lesions in mice. Furthermore gene expression studies uncovered that the tumour suppressive functions of miR-184 is possibly mediated by suppressing several members within the AKT/mTORC1 cascade, which inhibits the activation of S6K1, the key modulator of the protein synthesis pathway. Finally, miR-184 is only undetectable in triple-negative breast cancer (TNBC) patient samples. Epigenetic studies reveal that the miR-184 promoter is often epigenetically silenced in lymph node metastases of of a subset of TNBC patients, indicating a possible silencing mechanism. In summary, we have elucidated another layer of regulation in the PI3K/AKT/mTOR pathway. These findings uncover a potential therapeutic agent that could be used in combination with other inhibitors to treat TNBC.