Appetite for destruction: the inhibition of glycolysis as a therapy for tuberous sclerosis complex-related tumors. Editorial Article uri icon

Overview

abstract

  • 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.

publication date

  • October 21, 2011

Research

keywords

  • Glycolysis
  • Neoplasms
  • Tuberous Sclerosis

Identity

PubMed Central ID

  • PMC3198763

Scopus Document Identifier

  • 84859890862

Digital Object Identifier (DOI)

  • 10.1186/1741-7007-9-69

PubMed ID

  • 22018140

Additional Document Info

volume

  • 9