Research Papers:
Methylation-mediated silencing of microRNA-211 promotes cell growth and epithelial to mesenchymal transition through activation of the AKT/β-catenin pathway in GBM
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Abstract
Weidong Li1,*, Xiaobo Miao2,*, Lingling Liu3,*, Yue Zhang4,*, Xuejun Jin1, Xiaojun Luo5, Hai Gao6,7, Xubin Deng1
1Affiliated Cancer Hospital of Guangzhou Medical University, Guangzhou, China
2Department of Radiation and Chemotherapy Oncology, Ningbo No.2 Hospital, Ningbo, China
3Department of Hematology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China
4Department of Radiation Oncology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China
5Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou, China
6Xiamen Hospital of Traditional Chinese Medicine, Xiamen, China
7Xiamen Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Xiamen, China
*These authors have contributed equally to this work
Correspondence to:
Weidong Li, email: [email protected]
Hai Gao, email: [email protected]
Xubin Deng, email: [email protected]
Keywords: glioblastoma, miR-211, HMGA2, EZH2, epithelial to mesenchymal transition
Received: July 04, 2016 Accepted: January 23, 2017 Published: February 20, 2017
ABSTRACT
Aberrant expression of miR-211 has frequently been reported in cancer studies; however, its role in glioblastoma multiforme (GBM) has not been examined in detail. We investigated the function and the underlying mechanism of miR-211 in GBM. We revealed that miR-211 was downregulated in GBM tissues and cell lines. Restoration of miR-211 inhibited GBM cell growth and invasion both in vitro and in vivo. The epithelial to mesenchymal transition (EMT) phenotype was reversed when miR-211 expression was restored. HMGA2 was identified as a down-stream target of miR-211. MiR-211 had an inhibitory effect on AKT/β-catenin signaling, which was reversed by HMGA2 overexpression or miR-211 restoration. In addition, miR-211 was transcriptionally repressed by EZH2-induced H3K27 trimethylation and promoter methylation. Overall, our findings revealed miR-211 as a tumor suppressor in GBM and mir-211 may be a potential therapeutic target for GBM patients.
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PII: 15531