Glioblastomas are the most aggressive malignant glial tumors in adults. The median survival time is less than two years despite treatment. Glioblastoma cells use glucose as the major source of metabolic energy. Increased glucose consumption is usually associated with resistance to conventional anticancer therapy. Therefore, the rate of glucose metabolism is considered to be an important prognostic factor.

Interleukin-1β is a product of glial cells in response to hypoxia. In normal conditions, small amounts of interleukin-1β are produced constitutively. Interleukin-1β activates various glycolytic regulators such as nuclear factor ?B, mitogen-activated protein kinase, hypoxia-inducible factor 1 and p53. However, it was still unknown whether interleukin-1β affects the glucose metabolism in brain cells. Advanced glioblastomas mostly contain hypoxic areas due to the inadequate vascularisation. Thus, we suggest that interleukin-1β is upregulated in hypoxic glioblastomas and changes the glucose metabolic rate of the tumor cells.

To verify the hypothesis, we demonstrated that hypoxia enhances the expression of interleukin-1β in the glioblastoma cell line U87MG. Further, we studied the influence of interleukin-1β on the glucose metabolism in U87MG cells including glucose uptake and lactate release. Our findings provide new insights into the biology of glioblastomas.