Format

Send to

Choose Destination
Cell Death Dis. 2019 Jun 6;10(6):448. doi: 10.1038/s41419-019-1671-5.

Silencing of microRNA-708 promotes cell growth and epithelial-to-mesenchymal transition by activating the SPHK2/AKT/β-catenin pathway in glioma.

Author information

1
Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
2
Guangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, Southern Medical University, Guangzhou, China.
3
Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China.
4
Department of Emergency, Nanfang Hospital, Southern Medical University, Guangzhou, China.
5
Guangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, Southern Medical University, Guangzhou, China. Xiao_d@hotmail.com.
6
Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China. longh812@163.com.

Abstract

Aberrant microRNA-708 (miR-708) expression is frequently reported in cancer studies; however, its role in glioma has not been examined in detail. We investigated miR-708 function in glioma and revealed that miR-708 expression was significantly down-regulated in glioma tissues and cell lines. Restoration of miR-708 inhibited glioma cell growth and invasion both in vitro and in vivo. The oncogene SPHK2 (sphingosine kinase 2) was identified as a downstream target of miR-708 using luciferase and western blot assays. miR-708 inhibited AKT/β-catenin signaling, which is activated by SPHK2. In addition, we revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. In summary, our findings revealed that miR-708 is a glioma tumor suppressor and suggest that miR-708 is a potential therapeutic target for glioma patients.

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center