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Título

Direct targeting of Sec23a by miR-200s influences cancer cell secretome and promotes metastatic colonization

AutorCelià-Terrassa, Toni ; Kang, Yibin
Fecha de publicación2011
EditorNature Publishing Group
CitaciónNature Medicine 17(9): 1101-1109 (2011)
ResumenAlthough the role of miR-200s in regulating E-cadherin expression and epithelial-to-mesenchymal transition is well established, their influence on metastatic colonization remains controversial. Here we have used clinical and experimental models of breast cancer metastasis to discover a pro-metastatic role of miR-200s that goes beyond their regulation of E-cadherin and epithelial phenotype. Overexpression of miR-200s is associated with increased risk of metastasis in breast cancer and promotes metastatic colonization in mouse models, phenotypes that cannot be recapitulated by E-cadherin expression alone. Genomic and proteomic analyses revealed global shifts in gene expression upon miR-200 overexpression toward that of highly metastatic cells. miR-200s promote metastatic colonization partly through direct targeting of Sec23a, which mediates secretion of metastasis-suppressive proteins, including Igfbp4 and Tinagl1, as validated by functional and clinical correlation studies. Overall, these findings suggest a pleiotropic role of miR-200s in promoting metastatic colonization by influencing E-cadherin-dependent epithelial traits and Sec23a-mediated tumor cell secretome. © 2011 Nature America, Inc. All rights reserved.
DescripciónEl pdf del artículo es el manuscrito de autor.-- et al.
Versión del editorhttp://dx.doi.org/10.1038/nm.2401
URIhttp://hdl.handle.net/10261/52266
DOI10.1038/nm.2401
Identificadoresdoi: 10.1038/nm.2401
issn: 1078-8956
e-issn: 1546-170X
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