Nuclear receptor LXR as a novel therapeutic antitumoral target in glioblastoma

Antonio Moschetta

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)381-382
Number of pages2
JournalCancer Discovery
Volume1
Issue number5
DOIs
Publication statusPublished - Oct 2011

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LDL Receptors
Glioblastoma
Cytoplasmic and Nuclear Receptors
Cholesterol
Sterol Regulatory Element Binding Protein 1
Growth
Epidermal Growth Factor Receptor
Cell Death
Therapeutics
Mutation
Neoplasms

ASJC Scopus subject areas

  • Oncology

Cite this

Nuclear receptor LXR as a novel therapeutic antitumoral target in glioblastoma. / Moschetta, Antonio.

In: Cancer Discovery, Vol. 1, No. 5, 10.2011, p. 381-382.

Research output: Contribution to journalArticle

Moschetta, Antonio. / Nuclear receptor LXR as a novel therapeutic antitumoral target in glioblastoma. In: Cancer Discovery. 2011 ; Vol. 1, No. 5. pp. 381-382.
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