Department of Cell Biology, Harvard Medical School, 240 Longwood Ave, Boston, MA 02115, USA.
BMC Biol. 2011 Oct 21;9:69. doi: 10.1186/1741-7007-9-69.
The elevated metabolic requirements of cancer cells reflect their rapid growth and proliferation and are met through mutations in oncogenes and tumor suppressor genes that reprogram cellular processes. For example, in tuberous sclerosis complex (TSC)-related tumors, the loss of TSC1/2 function causes constitutive mTORC1 activity, which stimulates glycolysis, resulting in glucose addiction in vitro. In research published in Cell and Bioscience, Jiang and colleagues show that pharmacological restriction of glucose metabolism decreases tumor progression in a TSC xenograft model.
癌细胞代谢需求的增加反映了它们的快速生长和增殖，这是通过癌基因和肿瘤抑制基因的突变来实现的，这些突变重新编程了细胞过程。例如，在结节性硬化症（TSC）相关肿瘤中，TSC1/2 功能的丧失导致 mTORC1 活性的持续激活，从而刺激糖酵解，导致体外葡萄糖成瘾。在发表在《Cell and Bioscience》上的研究中，蒋和他的同事们表明，葡萄糖代谢的药理学限制可减少 TSC 异种移植模型中的肿瘤进展。
