The TCA cycle intermediate Isocitrate dehydrogenase commonly undergoes point mutations in cancers. This allows IDH to reduce a-Ketogluterate to 2Hydoxygluterate, causing a reduction in pVHLs ability to hydroxylate HIF-1a, and a subsequent accumulation of HIF-1a. This leads to angiogenesis via VEGF. If the cancer cell is converting its a-KG away form the TCA cycle, how does the cell make up for the loss of TCA function, and subsequent ETC function for energy production? Why would the cancer cell prefer to lose high yield energy production in exchange for low yield energy production?
Rapidly proliferating tissues (esp tumours) rewire their energy metabolism anyway to aerobic glycolysis where you have energy being produced by lactic acid fermentation even if oxygen is present. This is called the Warburg effect.Here's the thing about "low yield" though - glycolysis chucks out less ATP per reaction at the end, but you can crunch through a lot more ATP by just having more of it going on.
Secondly, hypoxia in a tumour is generally rate limiting, and therefore the shunting away of alpha-KG with the consequence of increased angiogenesis is good for the tumour.
the loss of function mutation of IDH does not necessary mean that the oxidative phosphorylation ceases. The supply of TCA intermediates can still be maintained if other pathways are upregulated, e.g. amino acid degradation. One has to keep in mind, that the TCA is not solely standing, but there is a highly dynamic network with many entry gates (illustrated in http://www.cs.cmu.edu/~blmt/Seminar/SeminarMaterials/kegg.gif). If you are interested in, the group of Eyal Gottlieb (http://www.beatson.gla.ac.uk/cancer-metabolism-growth-and-survival/eyal-gottlieb-apoptosis-and-tumour-metabolism.html) is investigating the metabolomics in cancer cells with truncated ability to run TCA. For example the showed upregulation of Acetyl-Synthetase 2 allowing acetate usage for cancer cell growth under metabolic stress.
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