The editorial concerns the article "Direct targeting of Sec23a by miR-200 affects the secretome of cancer cells and promotes metastatic colonization", published in Nature Medicine in 2011 (doi: 10.1038/nm.2401).[1][2] The article reports that overexpression of miR-200 is associated with an increased risk of metastasis in breast cancer and promotes metastatic colonization in mouse models.[1][2] MiR-200s directly target Sec23a, which affects the secretion of metastasis suppressor proteins such as Igfbp4 and Tinagl1.[1][2] These changes in the secretome of cancer cells contribute to metastatic colonization in addition to regulating E-cadherin and the epithelial phenotype.[1][2] Low expression of Sec23a correlates with shorter recurrence without metastasis (P = 0.0236).[1] A study confirmed decreased expression of Sec23a in breast and bladder cancer cell lines after miR-200.[1] Findings suggest a pleiotropic role of miR-200s in metastasis through secretome and cellular properties.[2]