MiR-145 inhibits tumor angiogenesis and growth by N-RAS and VEGF

MiR-145 is known as a tumor suppressor in numerous human cancers. However, its role in tumor angiogenesis remains poorly defined. In this study, we found that miR-145 was significantly downregulated in breast cancer tissues by using 106 cases of normal and cancer tissues as well as in breast cancer...

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Published in:Cell cycle (Georgetown, Tex.) Tex.), 2012-06, Vol.11 (11), p.2137-2145
Main Authors: Zou, Chao, Xu, Qing, Mao, Feng, Li, Dan, Bian, Chuanxiu, Liu, Ling-Zhi, Jiang, Yue, Chen, Xiaona, Qi, Yanting, Zhang, Xiaolong, Wang, Xuejing, Sun, Qiang, Kung, Hsiang-Fu, Lin, Marie C., Dress, Andreas, Wardle, Fiona, Jiang, Bing-Hua, Lai, Lihui
Format: Article
Language:English
Subjects:
angiogenesis
Animals
Binding
Biology
Bioscience
breast cancer
Breast Neoplasms - metabolism
Breast Neoplasms - pathology
Calcium
Cancer
Cell
Cell Line, Tumor
Cell Proliferation
Cell Survival
Cycle
Down-Regulation
Female
Humans
Landes
Mice
MicroRNAs - metabolism
miR-145
N-RAS
Neovascularization, Pathologic
Organogenesis
Proteins
ras Proteins - metabolism
Transplantation, Heterologous
Vascular Endothelial Growth Factor A - metabolism
VEGF-A
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Summary:MiR-145 is known as a tumor suppressor in numerous human cancers. However, its role in tumor angiogenesis remains poorly defined. In this study, we found that miR-145 was significantly downregulated in breast cancer tissues by using 106 cases of normal and cancer tissues as well as in breast cancer cells. MiR-145 exhibited inhibitory role in tumor angiogenesis, cell growth and invasion and tumor growth through the post-transcriptional regulation of the novel targets N-RAS and VEGF-A. In addition, we provide evidence that the expression levels of miR-145 correlate inversely with malignancy stages of breast tumors, although there is no association between miR-145 levels and hormone receptor levels in breast cancer. Taken together, these results demonstrate that miR-145 plays important inhibitory role in breast cancer malignancy by targeting N-RAS and VEGF-A, which may be potential therapeutic and diagnostic targets.
ISSN:1538-4101
1551-4005
DOI:10.4161/cc.20598