Nuclear receptor LXR as a novel therapeutic antitumoral target in glioblastoma

Cancer Discov. 2011 Oct;1(5):381-2. doi: 10.1158/2159-8290.CD-11-0228.

Abstract

Both primary and transformed cells need cholesterol for their growth. Guo and colleagues unraveled the connection between epidermal growth factor receptor mutations in glioblastoma and increased cholesterol influx via sterol regulatory element-binding protein 1 and low-density lipoprotein receptor (LDLR) increase. They propose the activation of the liver X receptor-inducible degrader of LDLR-LDLR axis as a therapeutic approach to reduce intracellular cholesterol, block tumor growth, and induce cell death.

MeSH terms

  • Cell Death / drug effects
  • Cell Death / genetics
  • Cholesterol / genetics
  • Cholesterol / metabolism
  • ErbB Receptors / genetics
  • ErbB Receptors / metabolism
  • Glioblastoma / drug therapy*
  • Glioblastoma / genetics
  • Glioblastoma / metabolism*
  • Glioblastoma / pathology
  • Humans
  • Ligands
  • Liver X Receptors
  • Molecular Targeted Therapy / methods
  • Mutation
  • Orphan Nuclear Receptors / genetics
  • Orphan Nuclear Receptors / metabolism*
  • Receptors, LDL / genetics
  • Receptors, LDL / metabolism
  • Sterol Regulatory Element Binding Protein 1 / genetics
  • Sterol Regulatory Element Binding Protein 1 / metabolism

Substances

  • Ligands
  • Liver X Receptors
  • Orphan Nuclear Receptors
  • Receptors, LDL
  • Sterol Regulatory Element Binding Protein 1
  • Cholesterol
  • ErbB Receptors