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Abstract
BackgroundGlucose metabolic reprogramming is a significant hallmark of malignant tumors including GBM. Previous studies suggest that microRNAs play key roles in modulating this process in GBM cells. miR-181b acts as a tumor suppressor miRNA in influencing glioma tumorigenesis. Our previous results showed that miR-181b was down-regulated in glioma cells and tissues.MethodsThe extracellular acidification rate (ECAR), colony formation assay and levels of Glut1 and PKM2 were measured to assess the glucose metabolic and proliferation changes in GBM cells overexpressing miR-181b. Immunoblotting and luciferase reporter assay were performed to confirm the expression and role of SP1 as a direct target of miR-181b. ChIP assay was used to figure out the transcriptional regulation of SP1 on Glut1 and PKM2. In vivo study was examined for the role of miR-181b in GBM cells.ResultsMiR-181b overexpression significantly reduced the glucose metabolic and colony formation ability of GBM cells. And, SP1 was confirmed as a direct target of miR-181b while upregulation of SP1 could reverse the influence of overexpression of miR-181b. Furthermore, Glut1 and PKM2 could be regulated by SP1. Finally, miR-181b could inhibit the tumor growth in vivo.ConclusionsOur article demonstrated the inhibitory effect of miR-181b on glucose metabolism and proliferation in GBM by suppressing SP1 expression.
Highlights
Glucose metabolic reprogramming is a significant hallmark of malignant tumors including Glioblastoma multiforme (GBM)
MiR‐181b suppresses the glucose metabolism and proliferation in GBM cells In our previous results, we confirmed that miR-181b was down-regulated in human GBM cells and tissues [18]
We investigate the role of miR-181b in GBM cells glucose metabolism and extracellular acidification rate (ECAR) was measured to assess the glycolysis rate
Summary
Glucose metabolic reprogramming is a significant hallmark of malignant tumors including GBM. Previous studies suggest that microRNAs play key roles in modulating this process in GBM cells. Our previous results showed that miR-181b was down-regulated in glioma cells and tissues. Glioblastoma multiforme (GBM), which is categorised as a WHO IV tumor, accounts for about half of glioma classification [2]. Warburg effect (aerobic glycolysis) represents major metabolic phenotypes for energy production. Lactate was produced from glucose metabolism in tumors cells, while normal differentiated cells extract energy via. It was reported that glycolytic metabolism of tumor tissues is three times higher than normal brain tissues [9]. There is still much need to investigate about how glucose metabolism in glioma is regulated
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