Appetite for destruction: the inhibition of glycolysis as a therapy for tuberous sclerosis complex-related tumors.
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.
Department of Cell Biology, Harvard Medical School, 240 Longwood Ave, Boston, MA 02115, USA.
Alfredo
A
Csibi
John
J
Blenis
D000818:Animals; D006019:Glycolysis; D006801:Humans; D009154:Mutation / Q000235:genetics; D009369:Neoplasms / Q000378:metabolism* / Q000628:therapy*; D015398:Signal Transduction; D014402:Tuberous Sclerosis / Q000378:metabolism*