Cancer cells often exhibit altered metabolism, commonly referred to as the Warburg effect, where they rely heavily on glycolysis for energy production, even in the presence of oxygen. PKM2 is a key player in this metabolic reprogramming. Unlike its highly active counterpart PKM1, PKM2 can switch between a high-activity tetrameric form and a low-activity dimeric form. The dimeric form of PKM2 allows the accumulation of glycolytic intermediates, which are then shunted into biosynthetic pathways essential for rapid cell proliferation.
