Warburg effect is one the halmarks of cancer. There are basically 3 facts you should know:
1) Most energy produced by cancerous cells is via glycolysis, followed by lactic acid fermentation; essentially anaerobic respiration as opposed to traditional aerobic respiration in non cancerous cells.
2) the rate at which respiration is occurring is much faster for cancerous cells than non-cancerous cells.
3) Low oxygen content in tumors
This should be a start for you
Warburg effect is one the halmarks of cancer. There are basically 3 facts you should know:
1) Most energy produced by cancerous cells is via glycolysis, followed by lactic acid fermentation; essentially anaerobic respiration as opposed to traditional aerobic respiration in non cancerous cells.
2) the rate at which respiration is occurring is much faster for cancerous cells than non-cancerous cells.
3) Low oxygen content in tumors
This should be a start for you
Please state a specific question, this is what Research Gate is for. Otherwise have a look at papers or even wikipedia to get an idea.
http://en.wikipedia.org/wiki/Warburg_effect
You'll find a simple lay-person's explanation here, and a little on some of the latest research into this clinically significant effect:
http://www.ludwigcancerresearch.org/news/targeting-cancers-sweet-tooth
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 because they are involved in the cell's apoptosis program which would otherwise kill cancerous 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 aerobic glycolytic rates to an overexpressed 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
The following explanation is cited from JECCR Review entitled as "Metabolic reprogramming: the emerging concept and associated therapeutic strategies."
In 1924, Otto Warburg discovered that tumor cells tend to produce large amounts of lactate from glucose, regardless of the available oxygen level [15, 16]. This situation is similar to anaerobic glycolysis, implying that oxidative phosphorylation (OXPHOS) is replaced by glycolysis in normal differentiated cells under hypoxia [23, 24]. However, cancer cells appear to engage in glycolytic metabolism before they are exposed to hypoxic conditions [15, 16]. OXPHOS in mitochondria generates as many as 36 mol ATP from 1 mol glucose, whereas the conversion of glucose to pyruvate or lactate produces only 2 or 4 mol ATP, respectively [25, 26]. It remains unclear why cancer cells largely depend on this “inefficient” metabolic pathway, even when enough oxygen is available [27, 28]. In striking contrast to normal cells, cancer cells preferentially uptake and convert glucose into lactate even in the presence of sufficient oxygen [29]. This seemingly “inefficient” metabolic characteristic relies largely on aberrant upregulation of GLUT1, a glucose transporters abundantly expressed in cancer cells [30, 31], although one contradictory study reported that GLUT1 is not necessarily involved in the Warburg effect depending on the degree of tumor invasiveness [32]. Inefficient ATP synthesis becomes an obstacle for cancer cells only when their energy resources are scarce. However, this is not the case in proliferating cancer cells with aberrant angiogenesis [29]. Tumor cells finely regulate ATP synthesis by regulating substrate uptake, as well as enzymes related to glycolysis, which enables them adapt to the nutrient microenvironment [33]. Moreover, the regulation of adenosine monophosphate-activated protein kinase (AMPK) signal transduction, a sensor of energy status, is intimately connected to the Warburg effect, one form of metabolic reprogramming of cancer cells [34, 35]. Indeed, genetic ablation of AMPK activates mammalian target of rapamycin (mTOR) signal with ectopic expression of hypoxia-inducible factor-1 alpha (HIF-1 alpha), resulting in rapid cellular proliferation accompanied by activation of aerobic glycolysis [35]. This strongly suggests the importance of cancer metabolic reprogramming in maintaining the interaction between the oxygen-sensing transcription factor and the nutrient-sensing signal pathway.
http://jeccr.biomedcentral.com/articles/10.1186/s13046-015-0221-y
It helps you to monitor the effect of chemicals as function of oxygen, carbon dioxide, glycolysis, energy released and conserved.
Most cancer cells are characterized by increased glucose uptake and aerobic glycolysis. A very high rate of glycolysis followed by lactic acid fermentation, even in the presence of oxygen and fully functioning mitochondria is known as the aerobic glycolysis (or ‘ Warburg effect’). Increased aerobic glycolysis is uniquely observed in cancer cells. It was Otto Warburg who demonstrated in 1924 that cancer cells show an increased dependence on glycolysis to meet their energy needs, regardless of whether they were well-oxygenated. Converting glucose to lactate, rather than metabolizing it through oxidative phosphorylation in the mitochondria, is far less effi cient as less ATP is generated per unit of glucose metabolized. Nevertheless, cancer cells perform aerobic glycolysis. Therefore, a high rate of glucose uptake is required to meet increased energy needs to support rapid tumor progression.
Previously, it was thought the Warburg effect was a consequence of damage to the mitochondria or an adaptation to hypoxic conditions during the early avascular phase of tumor development. But this hypothesis has been shown to be incorrect. In the last 90 years several hypotheses have been suggested, to this date, there is no clear explanation of this rather unusual effect.
The Warburg effect (not to be confused with the Warburg hypothesis) describes the phneomenon if FERMENTATION of pyruvate (conversion into lactate) instead of fully OXIZIDING it via the TCA an ETS even at physiological oxygenconcentrations. It has nothing to to with increased glycolysis since glycolysis only describes the process that starts from glucose and ends with pyruvate. It is whar happens from then on.... so the term „aerobic glycolysis“ is totsllx misleading since glycolysis is by definition an aerobic process.... please get this one straight
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