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.
Highlights
Glioblastoma multiforme (GBM), the most common brain cancer in adults, is notorious for its diffuse invasion and resistance to treatment [1, 2]
We revealed that miR-211 was downregulated in glioblastoma multiforme (GBM) tissues and cell lines
We first examined the expression of miR-211 in GBM tissues and cell lines with the use of qRT-PCR
Summary
Glioblastoma multiforme (GBM), the most common brain cancer in adults, is notorious for its diffuse invasion and resistance to treatment [1, 2]. Major therapeutic improvements were made by combining neurosurgery, chemotherapy, and radiotherapy, the prognosis and survival rate for patients with GBM is poor [3]. The 5 year survival rate of GBM patients is less than 5% [4]. There is an urgent need to find new strategies for the treatment of GBM. MiRNAs contribute to diverse biological processes, and to the progression and metastasis of human cancers [7, 8]. Abnormal expression of miRNAs often leads to GBM progression
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
