The Role Of Pyruvate Kinase M2 In Aerobic Glycolysis Of Cancer Cells: Mechanisms And Potential Inhibitor

Abstract

Cancer is defined as the uncontrolled growth of cells that can spread to other parts of the body, leading to significant health issues and affecting the quality of life patients. One hallmark of cancer is its ability to reprogram metabolism to support rapid cell proliferation, even under adverse conditions such as low oxygen levels. This article aims to explore how cancer cells predominantly utilize aerobic glycolysis, converting glucose into lactate, a process known as the Warburg Effect. This metabolic shift allows cancer cells to quickly generate energy and produce necessary biomass, including NADH, which is vital for maintaining redox balance and supporting continued proliferation. Pyruvate Kinase M2 (PKM2) is highlighted as a primary regulator of aerobic glycolysis in cancer cells. It facilitates the conversion of phosphoenolpyruvate (PEP) to pyruvate, which is crucial for lactate production. The low affinity of PKM2 for this conversion contributes to the metabolic advantages that cancer cells exploit. The review emphasizes the potential of targeting PKM2 as a therapeutic strategy for cancer treatment. Inhibiting PKM2 could disrupt the metabolic pathways that cancer cells rely on, with studies indicating that high doses of docosahexaenoic acid (DHA) can reduce PKM2 expression, presenting a promising direction for future research.