Ma Wenzhe, Sung Ho Joong, Park Joon Y, Matoba Satoaki, Hwang Paul M
Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
J Bioenerg Biomembr. 2007 Jun;39(3):243-6. doi: 10.1007/s10863-007-9083-0.
The genetic basis of increased glycolytic activity observed in cancer cells is likely to be the result of complex interactions of multiple regulatory pathways. Here we review the recent evidence of a simple genetic mechanism by which tumor suppressor p53 regulates mitochondrial respiration with secondary changes in glycolysis that are reminiscent of the Warburg effect. The biological significance of this regulation of the two major pathways of energy generation by p53 remains to be seen.
癌细胞中观察到的糖酵解活性增加的遗传基础可能是多种调控途径复杂相互作用的结果。在此,我们综述了一种简单遗传机制的最新证据,即肿瘤抑制因子p53通过对糖酵解产生继发性改变来调节线粒体呼吸作用,这让人联想到瓦伯格效应。p53对这两种主要能量产生途径的调控所具有的生物学意义仍有待观察。