Attacking the supply wagons to starve cancer cells to death

FEBS Lett. 2016 Apr;590(7):885-907. doi: 10.1002/1873-3468.12121. Epub 2016 Mar 22.

Abstract

The constitutive anabolism of cancer cells not only supports proliferation but also addicts tumor cells to a steady influx of exogenous nutrients. Limiting access to metabolic substrates could be an effective and selective means to block cancer growth. In this review, we define the pathways by which cancer cells acquire the raw materials for anabolism, highlight the actionable proteins in each pathway, and discuss the status of therapeutic interventions that disrupt nutrient acquisition. Critical open questions to be answered before apical metabolic inhibitors can be successfully and safely deployed in the clinic are also outlined. In summary, recent studies provide strong support that substrate limitation is a powerful therapeutic strategy to effectively, and safely, starve cancer cells to death.

Keywords: autophagy; cancer; macropinocytosis; metabolism; nutrient transporter; sphingolipid.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / adverse effects
  • Antineoplastic Agents / therapeutic use
  • Autophagy* / drug effects
  • Caloric Restriction* / adverse effects
  • Energy Metabolism* / drug effects
  • Enzyme Inhibitors / adverse effects
  • Enzyme Inhibitors / therapeutic use
  • Humans
  • Lysosomes / drug effects
  • Lysosomes / enzymology
  • Lysosomes / metabolism
  • Membrane Transport Modulators / adverse effects
  • Membrane Transport Modulators / therapeutic use
  • Models, Biological*
  • Neoplasm Proteins / antagonists & inhibitors
  • Neoplasm Proteins / metabolism
  • Neoplasms / drug therapy*
  • Neoplasms / enzymology
  • Neoplasms / metabolism
  • Neoplastic Stem Cells / drug effects
  • Neoplastic Stem Cells / enzymology
  • Neoplastic Stem Cells / metabolism
  • Pinocytosis / drug effects

Substances

  • Antineoplastic Agents
  • Enzyme Inhibitors
  • Membrane Transport Modulators
  • Neoplasm Proteins