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Reverse Warburg effect
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Reverse Warburg effect : ウィキペディア英語版
Reverse Warburg effect

The reverse Warburg effect in human breast cancers was first proposed by Dr. Michael P. Lisanti and colleagues in 2009. According to this model, aerobic glycolysis (a.k.a. the Warburg Effect) actually takes place in tumor associated fibroblasts, and not in cancer cells.〔〔〔〔〔 The researchers termed this new idea “The Reverse Warburg Effect”, to distinguish it from the conventional Warburg Effect, which was originally thought to take place in epithelial cancer cells.
==Description==
This has important consequences for tumor growth and progression. Aerobic glycolysis in cancer associated fibroblasts results in the production of high-energy metabolites (such as lactate and pyruvate), which can then be transferred to adjacent epithelial cancer cells, which are undergoing oxidative mitochondrial metabolism. This would then result in increased ATP production in cancer cells, driving tumor growth and metastasis. Essentially, in this new paradigm, stromal fibroblasts are feeding cancer cells via the transfer of high-energy metabolites, via a monocarboxylate transporter (MCT).〔〔〔〔〔〔
These new findings reverse over 85 years of dogma surrounding cancer cell metabolism, and explain the lethality of a caveolin 1 (Cav-1) deficient tumor microenvironment. More specifically, a loss of Cav-1 in stromal fibroblasts drives onset of “The Reverse Warburg Effect”, due to the autophagic destruction of mitochondria (mitophagy) in these stromal cells. Cancer cells induce “The Reverse Warburg Effect” in adjacent stromal fibroblasts by using oxidative stress, to promote aerobic glycolysis, under conditions of normoxia.
The autophagic tumor stroma model of cancer proposes that epithelial cancer cells use oxidative stress as a “weapon” to extract recycled nutrients from adjacent stromal fibroblasts (i.e., connective tissue cells.〔〔〔〔〔〔〔〔〔〔

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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