Journal
NATURE COMMUNICATIONS
Volume 4, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms3427
Keywords
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Categories
Funding
- NIH [CA016672, CA109298, UH2TR000943-01, P50 CA083639, P50 CA098258, CA128797, RC2GM092599, U54 CA151668, U24CA143835]
- CPRIT [RP110595]
- Ovarian Cancer Research Fund, Inc.
- DOD [OC073399, W81XWH-10-1-0158, BC085265]
- Marcus Foundation, Red and CharlineMcCombs Institute for the Early Detection and Treatment of Cancer
- RGK Foundation
- Gilder Foundation,
- Estate of C.G. Johnson, Jr
- Blanton-Davis Ovarian Cancer Research Program
- Betty Anne Asche Murray Distinguished Professorship
- Vanderbilt SPORE [CA90949]
- NCI [CA009666, CA143883]
- Conquer Cancer Foundation ASCO Young Investigator Award
- DoCM Advanced Scholar Program
- NCI-DHHS-NIH [T32 CA101642]
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The miR-200 family is well known to inhibit the epithelial-mesenchymal transition, suggesting it may therapeutically inhibit metastatic biology. However, conflicting reports regarding the role of miR-200 in suppressing or promoting metastasis in different cancer types have left unanswered questions. Here we demonstrate a difference in clinical outcome based on miR-200's role in blocking tumour angiogenesis. We demonstrate that miR-200 inhibits angiogenesis through direct and indirect mechanisms by targeting interleukin-8 and CXCL1 secreted by the tumour endothelial and cancer cells. Using several experimental models, we demonstrate the therapeutic potential of miR-200 delivery in ovarian, lung, renal and basal-like breast cancers by inhibiting angiogenesis. Delivery of miR-200 members into the tumour endothelium resulted in marked reductions in metastasis and angiogenesis, and induced vascular normalization. The role of miR-200 in blocking cancer angiogenesis in a cancer-dependent context defines its utility as a potential therapeutic agent.
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