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Direct targeting of Sec23a by miR-200s influences cancer cell secretome and promotes metastatic colonization
Open accessAbstract
Although 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.
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Metadata
- Authors
- Korpal, M., Ell, B. J., Buffa, F. M., Ibrahim, T., Blanco, M. A., Celià-Terrassa, T., Mercatali, L., Khan, Z., Goodarzi, H., Hua, Y., Wei, Y., Hu, G., Garcia, B. A., Ragoussis, J., Amadori, D., Harris, A. L., & Kang, Y.
- Venue
- Nature Medicine
- Published
- 2011-08-07
- Volume
- 17
- Issue
- 9
- Pages
- 1101-1108
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2138885372
- Cited by
- 636
- References
- 9
- FWCI
- 20.90
- Type
- journal article
- Language
- en
- Open access
- green
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