appetite for destruction the inhibition of glycolysis as a therapy for tuberous sclerosis complex-related tumors毁灭的欲望抑制糖酵解作为治疗结节性硬化症复数相关肿瘤.pdfVIP

Csibi and Blenis BMC Biology 2011, 9:69 /1741-7007/9/69 CO M M E N TA R Y Open Access Appetite for destruction: the inhibition of glycolysis as a therapy for tuberous sclerosis complex-related tumors Alfredo Csibi and John Blenis* See research article: /content/1/1/34 The glucose appetite of tumors and its regulation Abstract by mTORC1 The elevated metabolic requirements of cancer cells Research eforts have sought to characterize tumor cell relect their rapid growth and proliferation and are metabolism since Otto Warburg’s observations in the met through mutations in oncogenes and tumor 1920s of the tendency of cancer cells to metabolize suppressor genes that reprogram cellular processes. For glucose into lactate despite suicient oxygen levels example, in tuberous sclerosis complex (TSC)-related (known as the Warburg efect or ‘aerobic glycolysis’). By tumors, the loss of TSC1/2 function causes constitutive contrast, most diferentiated cells primarily metabolize mTORC1 activity, which stimulates glycolysis, resulting glucose to carbon dioxide by oxidation of pyruvate in the in glucose addiction in vitro. In research published in mitochondrial tricarboxylic acid (TCA) cycle, a process Cell and Bioscience, Jiang and colleagues show that known as oxidative phosphorylation that requires far less pharmacological restriction of glucose metabolism glucose to generate the same amount of energy. he decreases tumor progression in a TSC xe