NDLI: miR-382 Inhibits Osteosarcoma Metastasis and Relapse by Targeting Y Box-Binding Protein 1

Content Provider	PubMed Central
Author	Xu, Meng Jin, Hua Xu, Cheng-xiong Sun, Bo Song, Zhi-gang Bi, Wen-zhi Wang, Yan
Copyright Year	2015
Abstract	Lung metastasis and relapse in osteosarcoma (OS) patients indicate poor prognosis. Here, we identified significantly decreased expression of miR-382 in highly metastatic OS cell lines and relapsed OS samples compared to their parental cell lines and primary OS samples, respectively. In addition, our clinical data showed that the miR-382 expression level was inversely associated with relapse and positively associated with metastasis-free survival in OS patients. The overexpression of miR-382 suppressed epithelial–mesenchymal transition (EMT) and metastasis. This overexpression also decreased the cancer stem cell (CSC) population and function in OS cells. In contrast, inhibition of miR-382 stimulated EMT and metastasis and increased CSC population in OS cells. In addition, our in vivo experiments showed that the overexpression of miR-382 inhibited CSC-induced tumor formation, and the combination of miR-382 with doxorubicin prevented disease relapse in OS patients. Furthermore, we demonstrated that miR-382 exerted its tumor-suppressing potential by directly targeting Y box-binding protein 1 (YB-1) in OS. Taken together, our findings suggest that miR-382 functions as a tumor suppressor function and that the overexpression of miR-382 is a novel strategy to inhibit tumor metastasis and prevent CSC-induced relapse in OS.
Related Links	http://dx.doi.org/10.1038/mt.2014.197
Ending Page	98
Page Count	10
Starting Page	89
File Format	PDF
ISSN	15250016
e-ISSN	15250024
Journal	Molecular Therapy
Issue Number	1
Volume Number	23
Language	English
Publisher	Nature Publishing Group
Publisher Date	2015-01-01
Access Restriction	Open
Rights Holder	Nature Publishing Group
Subject Keyword	Molecular Medicine Genetics Molecular Biology Pharmacology Drug Discovery Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Genetics Medicine Drug Discovery Molecular Biology Molecular Medicine Pharmacology

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