Journal
CANCER CELL
Volume 25, Issue 4, Pages 501-515Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2014.03.007
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Funding
- City of Hope Women's Cancer Program
- National Institutes of Health (NIH)/National Cancer Institute (NCI) [R01CA166020, R01CA163586]
- California Breast Cancer Research Program [17IB-0054]
- Breast Cancer Research Foundation-American Association for Cancer Research [12-60-26-WANG]
- National Key Basic Research Development Program (973 Program) of China [2012CB9333004]
- NIH/NCI [P30CA33572]
- Center for Cancer Research, NCI
- Celgene
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Cancer-secreted microRNAs (miRNAs) are emerging mediators of cancer-host crosstalk. Here we show that miR-105, which is characteristically expressed and secreted by metastatic breast cancer cells, is a potent regulator of migration through targeting the tight junction protein ZO-1. In endothelial monolayers, exosome-mediated transfer of cancer-secreted miR-105 efficiently destroys tight junctions and the integrity of these natural barriers against metastasis. Overexpression of miR-105 in nonmetastatic cancer cells induces metastasis and vascular permeability in distant organs, whereas inhibition of miR-105 in highly metastatic tumors alleviates these effects. miR-105 can be detected in the circulation at the premetastatic stage, and its levels in the blood and tumor are associated with ZO-1 expression and metastatic progression in early-stage breast cancer.
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