CircANKRD17 promotes glycolysis by inhibiting miR‐143 in breast cancer cells
Hong Chen, Lingfei Zhang, Lu Zhang, Ying Miao, Yun Xi, Mo‐Fang Liu, Min Zhang, Biao Li
Abstract
Glucose metabolic reprogramming, known as the Warburg effect, is one of the metabolic hallmarks of tumor cells. Cancer cells preferentially metabolize glucose by glycolysis rather than mitochondrial oxidative phosphorylation regardless of oxygen availability, but the regulatory mechanism underlying this switch has been incompletely understood. Here, we report that the circular RNA circ ankyrin repeat domain 17 (ANKRD17) functions as a key regulator for glycolysis to promote cell growth, migration, invasion, and cell-cycle progression in breast cancer (BC) cells. We further show that circANKRD17 acts to accelerate glycolysis in BC cells by acting as a sponge for miR-143 and in turn overrides the repressive effect of miR-143, a well-documented glycolytic repressor, on hexokinase 2 in BC cells, thus resulting in enhanced glycolysis in BC cells. These data suggest the circANKRD17-miR-143 cascade as a novel mechanism in controlling glucose metabolic reprogramming in BC cells and suggest circANKRD17 as a promising therapeutic target to interrupt cancerous glycolysis.