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【參考文獻(xiàn)】[1] Gillies RJ, Gatenby RA. Hypoxia and adaptive landscapes in the evolution of carcinogenesis[J]. Cancer Metastasis Rev, 2007,26(2):311317.[2] Warburg O. On the origin of cancer cells[ J]. Science, 1956, 123(3191): 309314.[3] Koppenol WH,Bounds Warburg effect and metabolic efficiency :recrunching the numbers[EB/OL].(20090914)[20110416].[4] Gatenby RA, Gillies RJ. Why do cancers have high aerobic glycolysis[J]. NatRev Cancer, 2004, 4(11): 891899.[5]Zhao FQ, Keating AF. Functional properties and genomics of glucose transports[J]. Curr Genomics,2007,8(2):113128.[6]Mathupala SP, Colen CB, Parajuli P,et al. Lactate and malignant tumors: a therapeutic target at the end stage of glycolysis[J]. Bioenerg Biomembr, 2007,39(1):7377.[7]Gottlieb RA, Giesing HA, Zhu JY, et al. Cell acidification in apoptosis: granulocyte colonystimulating factor delays programmed cell death in neutrophils by upregulating the vacuolar H+ATPase[J]. Proc Natl Acad Sci USA,1995,92(13):59655968.[8] Goel A,Mathupala SP, Pederson metabolism in that demethylation events play a role in activating type Ⅱ hexokinase gene expression [J]. Biol Chem,2003 :278(17)。具體的方法包括抑制葡萄糖轉(zhuǎn)運、直接抑制糖酵解、抑制HIF作用、抑制mTOR通路等多種途徑來治療腫瘤。TIGAR表達(dá)產(chǎn)物可降解2,6二磷酸果糖,而2,6二磷酸果糖可以激動糖酵解的發(fā)生,所以TIGAR可抑制糖酵解通路。腫瘤抑制蛋白p53在調(diào)節(jié)線粒體呼吸與糖酵解平衡間起重要作用。使腫瘤細(xì)胞中GLUT1表達(dá)增高,腫瘤細(xì)胞攝取葡萄糖增高,糖酵解增加[16]。腫瘤細(xì)胞線粒體DNA變異現(xiàn)象較為普遍。通過上調(diào)