My earlier video Warburg Effect in the below link
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In this video I have explained in brief about what is Reverse Warburg effect. I have also touched upon some of the hypothesis that explains why Reverse Warburg effect is seen in cancer cells. Reverse Warburg effect is two compartment metabolic model, in this cancer associated fibroblast or stromal cells will undergo metabolic remodelling to provide high energy fuel for cancer cells. How this metabolic reprogramming is done by cancer cells is explained in reverse Warburg effect.
In oncology, the Warburg effect refers to the observation that even in aerobic conditions, cancer cells tend to favor metabolism via glycolysis rather than the much more efficient oxidative phosphorylation pathway which is the preference of most other cells of the body. In tumor cells, the last product of glycolysis, pyruvate, is converted into lactate. The Warburg effect may simply be a consequence of damage to the mitochondria in cancer, or an adaptation to low-oxygen environments within tumors, or a result of cancer genes shutting down the mitochondria, which are involved in the cell's apoptosis program that kills cancer cells. It may also be an effect associated with cell proliferation. Since glycolysis provides most of the building blocks required for cell proliferation, cancer cells (and normal proliferating cells) have been proposed to need to activate glycolysis, despite the presence of oxygen, to proliferate. Evidence attributes some of the high anaerobic glycolytic rates to an over expressed form of mitochondrially bound hexokinase responsible for driving the high glycolytic activity. In kidney cancer, this effect could be due to the presence of mutations in the von Hippel–Lindau tumor suppressor gene upregulating glycolytic enzymes, including the M2 splice isoform of pyruvate kinase. TP53 mutation hits energy metabolism and increases glycolysis in breast cancer. The Warburg effect is associated with glucose uptake and utilization, as this ties into how mitochondrial activity is regulated. The concern lies less in mitochondrial damage and more in the change in activity. On the other hand, tumor cells exhibit increased rates of glycolysis which can be explained with mitochondrial damage. In March 2008, Lewis C. Cantley and colleagues announced that the tumor M2-PK, a form of the pyruvate kinase enzyme, gives rise to the Warburg effect. Tumor M2-PK is produced in all rapidly dividing cells and is responsible for enabling cancer cells to consume glucose at an accelerated rate; on forcing the cells to switch to pyruvate kinase's alternative form by inhibiting the production of tumor M2-PK, their growth was curbed. The researchers acknowledged the fact that the exact chemistry of glucose metabolism was likely to vary across different forms of cancer; however, PKM2 was identified in all of the cancer cells they had tested. This enzyme form is not usually found in healthy tissue, though it is apparently necessary when cells need to multiply quickly, e.g., in healing wounds or hematopoiesis.

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