Warburg Effect

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The anti-apoptotic mutations related to cytochrome c are not the only mechanisms acquired by cells in the development of a tumor. Another important hallmark of cancer is the alteration of cellular metabolism, also known as the Warburg Effect, which demonstrates an increased rate of glycolysis despite the presence of oxygen in tumor cells (Hallmarks). Due to the unlimited and uncontrollable division by tumorigenic cells, the Warburg Effect confers growth advantages compared to non-proliferating cells because it promotes the uptake of glucose, it produces less reactive oxygen species (ROS), and it generates ATP more rapidly than oxidative phosphorylation, all of which are considered to facilitate rapid growth and survival (1).
Besides inducing apoptosis and controlling the cell cycle, p53 has been demonstrated to be a central component and key regulator of the metabolic stress machinery. The metabolic balance between glycolysis and oxidative phosphorylation is heavily coordinated by p53 activity, which is activated by
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The TIGAR enzyme regulates glucose breakdown, DNA repair, and organelle degradation, protects cells from oxidative stress, and blocks glycolysis, thus redirecting metabolic intermediates into the anabolic pentose phosphate pathway (4). Therefore, the loss of SCO2 and TIGAR regulation by p53 mutations would impair the electron transport chain and promote the switch in ATP synthesis from oxidative phosphorylation to glycolysis, most likely providing a significant metabolic and proliferative advantage in tumorigenic cells (2). However, the complex roles of p53 in cellular regulatory pathways make it difficult to establish and summarize how p53 mutations directly induce these metabolic alterations in tumor cells
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