MicroRNA-9 (miR-9) is upregulated in breast cancer cells and directly targets the *CDH1* gene, leading to decreased expression of E-cadherin. This results in increased cell motility and invasiveness, as well as activation of β-catenin signaling, which upregulates vascular endothelial growth factor (VEGF) expression and promotes tumor angiogenesis. Overexpression of miR-9 in non-metastatic breast tumor cells enables them to form pulmonary micrometastases in mice. Conversely, inhibiting miR-9 using a 'miRNA sponge' in highly malignant cells inhibits metastasis formation. miR-9 expression is activated by MYC and MYCN, which directly bind to the *mir-9-3* locus. In human cancers, miR-9 levels correlate with *MYCN* amplification, tumor grade, and metastatic status. These findings uncover a regulatory and signaling pathway involving a metastasis-promoting miRNA that directly targets the key metastasis-suppressing protein E-cadherin.MicroRNA-9 (miR-9) is upregulated in breast cancer cells and directly targets the *CDH1* gene, leading to decreased expression of E-cadherin. This results in increased cell motility and invasiveness, as well as activation of β-catenin signaling, which upregulates vascular endothelial growth factor (VEGF) expression and promotes tumor angiogenesis. Overexpression of miR-9 in non-metastatic breast tumor cells enables them to form pulmonary micrometastases in mice. Conversely, inhibiting miR-9 using a 'miRNA sponge' in highly malignant cells inhibits metastasis formation. miR-9 expression is activated by MYC and MYCN, which directly bind to the *mir-9-3* locus. In human cancers, miR-9 levels correlate with *MYCN* amplification, tumor grade, and metastatic status. These findings uncover a regulatory and signaling pathway involving a metastasis-promoting miRNA that directly targets the key metastasis-suppressing protein E-cadherin.