Abstract

Warburg effect is characterized by an increased utilization of glucose via glycolysis in cancer cells, even when enough oxygen is present to properly respire. Recent studies demonstrate that deregulation of microRNAs contributes to the Warburg effect. In the present study, we show that miR-144 is downregulated while glucose transporter 1 (Glut1) is upregulated in ovarian cancers. In vitro studies further showed that miR-144 inhibits Glut1 expression through targeting its 3'-untranslated region. As a result, cells overexpressing miR-144 exhibited a metabolic shift, including enhanced glucose uptake and lactate production. The altered glucose metabolism induced by miR-144 also leads to a rapid growth of ovarian cancer cells. Taken together, our results indicate that miR-144 may serve as a molecular switch to regulate glycolysis in ovarian cancer by targeting the expression of Glut1.

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