Regulation of aerobic glycolysis to decelerate tumor proliferation by small molecule inhibitors targeting glucose transporters

作者：Meng Gao, Jian Huang, Xin Jiang, Yafei Yuan, Huanhuan Pang, Shuchen Luo, Nan Wang, Chengbo Yao, Zuwan Lin, De-Bing Pu, Shuo Zhang, Pengcheng Sun, Zhuoyi Liu, Yu Xiao, Qian Wang, Zeping Hu, Hang Yin · 发表于：Protein & Cell · 年份：2020 · DOI：10.1007/s13238-020-00725-7 · 被引用次数：29 · 研究领域：Cancer, Hypoxia, and Metabolism、Metabolism, Diabetes, and Cancer、Cancer-related Molecular Pathways

Dear Editor, Different from normal differentiated cells, metabolic reprogramming was spotted in cancer cells, due to increased demand for energy and macromolecule synthesis during their rapid proliferation (Hanahan and Weinberg, 2011; Pavlova and Thompson, 2016). Most cancer cells prefer anaerobic glycolysis even with oxygen in the environment due to its higher speed to produce macromolecular materials required for biosynthesis (Vander Heiden et al., 2009; DeBerardinis and Chandel, 2016). But to compensate for the lower efficiency of anaerobic glycolysis in producing ATP, these cancer cells demand much higher glucose supply (Warburg, 1956; Vander Heiden et al., 2009). These metabolic characteristics point to the huge demand of cancer cells for carbohydrate substrates, which creates the possibility of treating tumors by exploiting this feature (Patra et al., 2013; DeBerardinis and Chandel, 2016). Importantly, glucose transporters (GLUTs), particularly GLUT1 and GLUT3, which deliver the carbohydrate substrate in both glycolysis and oxidative phosphorylation pathways, were found to be overexpressed in most cancer cells (Amann et al., 2009; Krzeslak et al., 2012). Consequently, the abnormally high expression of GLUT1 and GLUT3 has been suggested as a considerable factor affecting the deterioration of cancer (Younes et al., 1997; Haber et al., 1998). Based on these rationales, strategies such as ‘starving off the cancers’ have been entertained (Katt et al., 2019), nonetheless, lit...