Glucose Transporter Regulation in Cancer: A Profile and the Loops

Cancer cells are characterized by increased energy demand and glucose uptake. Glucose transporters (GLUTs) are regarded as one of the most important proteins controlling glycolytic flux. At the protein level, GLUTs are regulated both by expression and by translocation from intracellular compartments to the plasma membrane. Many oncogenic pathways, including phosphatidylinositol 3-kinase (PI3K)/Akt, mTOR, hypoxia-inducible factor as well as mutations of p53 and RAS, are involved in the regulation of GLUT function. Meanwhile, alteration of GLUT leads to subsequent changes that modulate the activity of canonical oncogenic pathways. This review provides a profile of the reciprocal regulation between GLUTs and relative pathways including PI3K/Akt, mTOR, HIF, RAS, MMP, p53. In addition, because inhibiting GLUTs have been shown to decrease cancer cell growth, we also focus on in vivo studies using GLUT as therapeutic targets of anticancer treatment.