MiR-215, an activator of the CTNNBIP1/β-catenin pathway, is a marker of poor prognosis in human glioma
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Yong-Qing Tong1,2, Bei Liu3, Hong-Yun Zheng2, Jian Gu1, Hang Liu2, Feng Li1, Bi-Hua Tan4, Melanie Hartman4, Chunhua Song4, Yan Li1,2
1Department of Clinical Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, PR China
2Clinical Molecular Diagnostic Center, Renmin Hospital of Wuhan University, Wuhan 430060, PR China
3Department of Pathology Affiliated Tianyou Hospital of Wuhan University of Science and Technology, Wuhan 430064, PR China
4Pennsylvania State University College of Medicine and Hershey Medical Center, Hershey, Pennsylvania 17033, USA
Yan Li, e-mail: [email protected]
Chunhua Song, e-mail: [email protected]
Keywords: miR-215, glioma, prognosis, CTNNBIP1, TGF-β1
Received: April 19, 2015 Accepted: July 08, 2015 Published: July 22, 2015
MicroRNA-215 (miR-215) promotes tumor growth in various human malignancies. However, its role has not yet been determined in human glioma. Here, we found that levels of miR-215 were higher in glioma tissues than in corresponding non-neoplastic brain tissue. High miR-215 expression was correlated with higher World Health Organization (WHO) grades and shorter overall survival. Multivariate and univariate analysis indicated that miR-215 expression was an independent prognostic factor. We also found that TGF-beta1, phosphorylated beta-catenin, alpha-SMA, and fibronectin were increased in glioma tissues. Additionally, CTNNBIP1, a direct target of miR-215, was decreased in glioma compared to adjacent normal tissue. These data indicate that miR-215 activates Wnt/β-catenin signaling by increasing β-catenin phosphorylation, α-SMA expression, and fibronectin expression. It promotes TGF-β1-induced oncogenesis by suppressing CTNNBIP1 in glioma. In summary, miR-215 is overexpressed in human glioma, is involved in TGF-β1-induced oncogenesis, and can be used as a marker of poor prognosis in glioma patients.
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