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Decreased miR-106a inhibits glioma cell glucose uptake and proliferation by targeting SLC2A3 in GBM

Dong-Wei Dai1, Qiong Lu2, Lai-Xing Wang1, Wen-Yuan Zhao1, Yi-Qun Cao1, Ya-Nan Li1, Guo-Sheng Han1, Jian-Min Liu1* and Zhi-Jian Yue1*

Author Affiliations

1 Department of Neurosurgery, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, China

2 Department of Laboratory Medicine, Changhai Hospital, Second Military Medical University, Shanghai China

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BMC Cancer 2013, 13:478  doi:10.1186/1471-2407-13-478

Published: 14 October 2013



MiR-106a is frequently down-regulated in various types of human cancer. However the underlying mechanism of miR-106a involved in glioma remains elusive.


The association of miR-106a with glioma grade and patient survival was analyzed. The biological function and target of miR-106a were determined by bioinformatic analysis and cell experiments (Western blot, luciferase reporter, cell cycle, ntracellular ATP production and glucose uptake assay). Finally, rescue expression of its target SLC2A3 was used to test the role of SLC2A3 in miR-106a-mediated cell glycolysis and proliferation.


Here we showed that miR-106a was a tumor suppressor miRNA was involved in GBM cell glucose uptake and proliferation. Decreased miR-106a in GBM tissues and conferred a poor survival of GBM patients. SLC2A3 was identified as a core target of miR-106a in GBM cells. Inhibition of SLC2A3 by miR-106a attenuated cell proliferation and inhibited glucose uptake. In addition, for each biological process we identified ontology-associated transcripts that significantly correlated with SLC2A3 expression. Finally, the expression of SLC2A3 largely abrogated miR-106a-mediated cell proliferation and glucose uptake in GBM cells.


Taken together, miR-106a and SLC2A3 could be potential therapeutic approaches for GBM.

miR-106a; SLC2A3; Cell proliferation; Glucose uptake; GBM