The metabolic pathway of glucose differs significantly between a normal cell and a cancerous cell. In normal cells, glucose is primarily metabolized through a process called cellular respiration, which includes glycolysis, the Krebs cycle also known as the citric acid cycle or TCA cycle , and oxidative phosphorylation. This process efficiently generates adenosine triphosphate ATP , the cell's primary energy source. In contrast, cancerous cells predominantly rely on a less efficient process called aerobic glycolysis, also known as the Warburg effect, even in the presence of oxygen.Here's a brief overview of the two metabolic pathways:1. Normal cells:- Glycolysis: Glucose is converted to pyruvate in the cytoplasm, generating a small amount of ATP and NADH.- Krebs cycle: Pyruvate is transported into the mitochondria, where it is converted to acetyl-CoA and enters the Krebs cycle. This generates more NADH, FADH2, and a small amount of ATP.- Oxidative phosphorylation: NADH and FADH2 donate electrons to the electron transport chain in the inner mitochondrial membrane, ultimately generating a large amount of ATP through the process of chemiosmosis.2. Cancerous cells Warburg effect :- Aerobic glycolysis: Glucose is rapidly converted to pyruvate in the cytoplasm, generating a small amount of ATP. However, instead of entering the mitochondria, pyruvate is converted to lactate and secreted from the cell. This process is less efficient in generating ATP but provides cancer cells with other advantages, such as faster energy production, increased biosynthesis of macromolecules, and an acidic microenvironment that promotes invasion and metastasis.Based on these differences, several potential targets can be identified for cancer treatment:1. Glucose transporters GLUTs : Inhibiting glucose uptake by cancer cells can limit their energy supply and biosynthesis capabilities. Drugs targeting GLUTs may selectively impair cancer cell growth.2. Glycolytic enzymes: Inhibiting key glycolytic enzymes, such as hexokinase, phosphofructokinase, or pyruvate kinase, can disrupt the Warburg effect and impair cancer cell metabolism.3. Lactate dehydrogenase LDH : Inhibiting LDH, which converts pyruvate to lactate, can force cancer cells to rely more on oxidative phosphorylation and potentially increase their sensitivity to mitochondrial-targeting therapies.4. Monocarboxylate transporters MCTs : Blocking MCTs, which are responsible for lactate export, can lead to intracellular lactate accumulation and disrupt the pH balance in cancer cells, potentially impairing their survival and growth.5. Mitochondrial metabolism: Targeting mitochondrial metabolism, such as the Krebs cycle or oxidative phosphorylation, can selectively impair energy production in cancer cells that are partially or fully reliant on these pathways.It is important to note that cancer cells are highly adaptable and can develop resistance to metabolic-targeting therapies. Therefore, a combination of therapies targeting multiple aspects of cancer cell metabolism may be necessary for effective treatment.