A growing body of evidence demonstrates that the oncogenic miRNAs are critical components that are involved in breastcancer (BC) progression. Thus, they are attracting a great deal of consideration as they provide opportunities for the novel avenues fordeveloping BC targeted therapy. In the current review, we try to discuss the key oncogenic miRNAs implicated in cell migration, invasionand metastasis (e.g., miR-9, miR-10b, miR-10b-5p, miR-17/9, miR-21, miR-103/107, miR-181b-1, miR-301, miR-301a, miR-373, miR-489, miR-495 and miR-520c), apoptosis inhibition (e.g., miR-21, miR-155, miR-181, miR-182 and miR-221/222), cell proliferation (e.g.,miR-221/222, miR-17/92, miR-21, miR-301a, miR-155, miR-181 b, miR-182, miR-214, miR-20b, miR-29a, miR-196, miR-199a-3p, miR-210, miR-301a, miR-375, miR-378-3p and miR-489), and angiogenesis (e.g., miR-9, miR-17/92 cluster, miR-93 and miR-210). In particular, here, we considered miRNA-based therapeutic approaches to summarize the evidence for their potential therapeutic uses in clinical practice. Therefore, miRNA mimics (i.e., replacement and restoration of miRNAs) and inhibition therapy (e.g., anti-miRNA oligonucleotides (AMO), antagomiRs or antisense oligonucleotides (ASOs): cholesterol-conjugated anti-miRs and locked nucleic acid (LNA)), miRNA sponges, nanoparticles (NPs), multiple-target anti-mirna antisense oligonucleotide technology (MTg-AMOs), and artificial miRNAs (amiRNAs) have been indicated throughout the article as much as possible.