期刊
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
卷 44, 期 11, 页码 1711-1717出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biocel.2012.06.027
关键词
Mir-410; Glioma; MET; AKT; Tumor suppressor
资金
- National High Technology Research and Development Program 863 [2012AA02A508]
- National 11th five years supporting project [2007BA105808]
- Heilongjiang natural science Key projects [CO3030307]
MET, the receptor for hepatocyte growth factor receptor (HGF), has been reported to trigger multiple and sometimes opposing cellular responses in various types of tumor cells. It has been implicated in the regulation of tumor-cell survival, proliferation, angiogenesis, invasion and metastasis. However, the MET regulatory mechanism in glioma is not well known. MicroRNAs are a class of small noncoding RNAs that play important roles in a variety of biological processes including human cancers. In this study, we used computational and expressional analysis to identify that the 'seed sequence' of miR-410 matched the 3 ' UTR of the MET mRNA. Besides, the expression of miR-410 was inversely associated with MET in human glioma tissues. Using luciferase and western blot assay, we certified that miR-410 directly targeted MET in glioma cells. While restoring expression of miR-410 led to proliferation inhibition and reduced invasive capability in glioma cells. Furthermore, we showed that miR-410 played an important role in regulating MET-induced AKT signal transduction. While downregulation of MET by RNAi, we observed that MET knockdown resulted in effects similar to that with miR-410 transfection in glioma cells. Our findings suggest that miR-410, a direct regulator of MET, may function as a tumor suppressor in human gliomas. Crown Copyright (C) 2012 Published by Elsevier Ltd. All rights reserved.
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