Figure 4.

Glycolysis-induced autophagy in the presence of glucose starvation. Stimuli, either tumor cell-autonomous or from the TME (extracellular) increase the expression and/or activity of one or more glycolytic components (transporters, enzymes or metabolites). In the presence of glucose deprivation, however, unoccupied glycolytic enzymes (e.g., ALDO, GAPDH) or decreased levels of glycolytic metabolites (e.g., DHAP) lead to AMPK activation through various mechanisms (see text for details). ALDO, aldolase, fructose-bisphosphate; AMPK, adenosine monophosphate-activated protein kinase; DHAP, dihydroxyacetone phosphate; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; mTORC1, mechanistic target of rapamycin complex 1.