| Literature DB >> 24735924 |
Weiying Zhou1, Miranda Y Fong2, Yongfen Min3, George Somlo4, Liang Liu5, Melanie R Palomares6, Yang Yu5, Amy Chow2, Sean Timothy Francis O'Connor2, Andrew R Chin7, Yun Yen8, Yafan Wang9, Eric G Marcusson10, Peiguo Chu11, Jun Wu12, Xiwei Wu13, Arthur Xuejun Li14, Zhuo Li15, Hanlin Gao16, Xiubao Ren17, Mark P Boldin18, Pengnian Charles Lin3, Shizhen Emily Wang19.
Abstract
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.Entities:
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Year: 2014 PMID： 24735924 PMCID： PMC4016197 DOI： 10.1016/j.ccr.2014.03.007
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743