期刊
BREAST CANCER RESEARCH AND TREATMENT
卷 137, 期 2, 页码 373-382出版社
SPRINGER
DOI: 10.1007/s10549-012-2346-4
关键词
miR-30c; Breast tumor invasion; TWF1; VIM; IL-11
类别
资金
- University of Chicago Women's Board
- National Institutes of Health (NIH) [DK070103-05]
- Department of Defense Breast Cancer Research Program [W81XWH-09-1-0331]
- Paul Calabresi K12 Award [1K12CA139160-02]
- NCI [K99 CA160638-01A1]
- Chicago Fellows Program at the University of Chicago
- University of Chicago Clinical and Translational Science Award [UL1 RR024999]
- Sociedad Espanola de Oncologia Medica (SEOM)
- Breast SPORE at University of North Carolina [5-P50-CA58223-17]
- Breast SPORE at the University of Chicago [P50CA125183-05]
- Doris Duke Charitable Foundation
- University of Chicago Cancer Research Center Pilot Fund
- BSD Imaging Research Institute Pilot Research Projects Using Animal Imaging
- UCMC/Northshore Collaborative Funds
- Carole and Gordon Segal Grant
- Virginia and D. K. Ludwig Fund
- NIH [U54 CA 126524, P01 CA139490]
- Breast Cancer Research Foundation
- University of Chicago Cancer Center Support Grant [CA 014599]
Metastasis remains a significant challenge in treating cancer. A better understanding of the molecular mechanisms underlying metastasis is needed to develop more effective treatments. Here, we show that human breast tumor biomarker miR-30c regulates invasion by targeting the cytoskeleton network genes encoding twinfilin 1 (TWF1) and vimentin (VIM). Both VIM and TWF1 have been shown to regulate epithelial-to-mesenchymal transition. Similar to TWF1, VIM also regulates F-actin formation, a key component of cellular transition to a more invasive mesenchymal phenotype. To further characterize the role of the TWF1 pathway in breast cancer, we found that IL-11 is an important target of TWF1 that regulates breast cancer cell invasion and STAT3 phosphorylation. The miR-30c-VIM/TWF1 signaling cascade is also associated with clinical outcome in breast cancer patients.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据