| First Author | Martello G | Year | 2010 |
| Journal | Cell | Volume | 141 |
| Issue | 7 | Pages | 1195-207 |
| PubMed ID | 20603000 | Mgi Jnum | J:167941 |
| Mgi Id | MGI:4881385 | Doi | 10.1016/j.cell.2010.05.017 |
| Citation | Martello G, et al. (2010) A MicroRNA targeting dicer for metastasis control. Cell 141(7):1195-207 |
| abstractText | Although specific microRNAs (miRNAs) can be upregulated in cancer, global miRNA downregulation is a common trait of human malignancies. The mechanisms of this phenomenon and the advantages it affords remain poorly understood. Here we identify a microRNA family, miR-103/107, that attenuates miRNA biosynthesis by targeting Dicer, a key component of the miRNA processing machinery. In human breast cancer, high levels of miR-103/107 are associated with metastasis and poor outcome. Functionally, miR-103/107 confer migratory capacities in vitro and empower metastatic dissemination of otherwise nonaggressive cells in vivo. Inhibition of miR-103/107 opposes migration and metastasis of malignant cells. At the cellular level, a key event fostered by miR-103/107 is induction of epithelial-to-mesenchymal transition (EMT), attained by downregulating miR-200 levels. These findings suggest a new pathway by which Dicer inhibition drifts epithelial cancer toward a less-differentiated, mesenchymal fate to foster metastasis. |
