Figure 4. Regulation of the cell cycle in cancer by metabolic/signaling mechanism.

High levels of intracellular fructose 6-P fuel the hexosamine pathway by generating substrates (UDP-GlcNAc) for MGAT5. The products (β1,6 branched N-glycans) interact with galectins, which promote stabilization growth factor receptors on the cell surface. The stimulation of high-N-glycan or low-N-glycan receptors triggers opposite signaling that promotes G1/S progression or G1 arrest, respectively. This schematic representation is adapted from [27].