Figure 3.

Schematic representation of the effects of HKDC1 over-expression in cancer cells. The cell membrane glucose transporters (GLUT 1/3) mediate the glucose uptake, which is degraded to pyruvate by glycolysis. Upregulation of HKDC1 (and other HKs) in many cancer types leads to enhanced generation of glycolytic intermediate, which functions as precursors for numerous metabolic pathways necessary for the biosynthesis of cellular components; pentose phosphate pathway (marked with thick red arrows), cholesterol biosynthesis, and fatty acid biosynthesis. Notably, HKDC1 upregulation leads to an increase in HKDC1-mitochondrial binding, which is responsible for the maintenance of glycolysis and TCA cycle and contributes to unabated cell proliferation through the aversion of apoptosis and endoplasmic reticulum (ER)-mediated stress response mechanisms by reducing the number of physical contact points between ER and mitochondria.