Glucose metabolism in cancer cells

被引:174
作者
Annibaldi, Alessandro [1 ]
Widmann, Christian [1 ]
机构
[1] Univ Lausanne, Dept Physiol, CH-1005 Lausanne, Switzerland
基金
瑞士国家科学基金会;
关键词
apoptosis; cancer; glucose; glycolysis; oncogene; DEPENDENT ANION CHANNEL; HEXOKINASE-II; TUMOR-CELLS; INDUCED CYTOTOXICITY; AEROBIC GLYCOLYSIS; ENERGY-METABOLISM; BREAST-CANCER; PH; MITOCHONDRIA; HYPOXIA;
D O I
10.1097/MCO.0b013e32833a5577
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review Cancer cells alter their metabolism in order to support their rapid proliferation and expansion across the body. In particular, tumor cells, rather than fueling glucose in the oxidative phosphorylation pathway, generally use glucose for aerobic glycolysis. In this review, we discuss some of the mechanisms thought to be responsible for the acquisition of a glycolytic phenotype in cancer cells and how the switch towards glycolysis represents a selective growth advantage. Recent findings Glucose deprivation can activate oncogenes and these can upregulate proteins involved in aerobic glycolysis. In turn, proteins implicated in increased glycolysis can render tumor cells more resistant to apoptosis. Aerobic glycolysis induces acidification of the tumor environment, favoring the development of a more aggressive and invasive phenotype. Altering the pH around tumors might represent a way to hamper tumor development as suggested by a recent work demonstrating that bicarbonate, which increases the pH of tumors, prevented spontaneous metastatization. Summary The acquisition of a glycolytic phenotype by transformed cells confers a selective growth advantage to these cells. Interfering with aerobic glycolysis, therefore, represents a potentially effective strategy to selectively target cancer cells.
引用
收藏
页码:466 / 470
页数:5
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