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LXR-α selectively reprogrammes cancer cells to enter into apoptosis.

Abstract
There exists a general recognition of the fact that LXR-α, being a member of the nuclear receptor family, plays a crucial role in the biological process that connects inflammation, cholesterol homeostasis, and cellular decisions. In this context the present study was addressed to understand the role of LXR-α gene in the selective and specific reprogramming of cancer cells into a state of apoptosis leaving the normal cells unaffected. The results of this study revealed that LXR-α gene when activated in cancerous cells of diverse origin results in the regulation of genes coding for Bcl-2, AATF, and Par-4 in a fashion, forcing these cells to enter into the state of apoptosis leaving the normal cells unaffected. On the basis of this study we propose that in near future LXR-α agonist (Withaferin A) may definitely find its use in the therapeutic interventions directed towards the treatment of cancer.
AuthorsAanchal Mehrotra, Deepak Kaul, Kusum Joshi
JournalMolecular and cellular biochemistry (Mol Cell Biochem) Vol. 349 Issue 1-2 Pg. 41-55 (Mar 2011) ISSN: 1573-4919 [Electronic] Netherlands
PMID21125317 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antineoplastic Agents
  • Basic Helix-Loop-Helix Transcription Factors
  • E2F1 Transcription Factor
  • E2F1 protein, human
  • Hydroxycholesterols
  • Ligands
  • Liver X Receptors
  • MXI1 protein, human
  • NR1H3 protein, human
  • Orphan Nuclear Receptors
  • Sterol Regulatory Element Binding Protein 1
  • Tumor Suppressor Proteins
  • Withanolides
  • withaferin A
Topics
  • Antineoplastic Agents (pharmacology)
  • Apoptosis (drug effects)
  • Basic Helix-Loop-Helix Transcription Factors (genetics)
  • Cell Cycle (drug effects)
  • Cell Line, Tumor
  • Cell Survival (drug effects)
  • E2F1 Transcription Factor (genetics)
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Genes, Reporter
  • Humans
  • Hydroxycholesterols (pharmacology)
  • Ligands
  • Liver X Receptors
  • Neoplasms (metabolism, pathology)
  • Orphan Nuclear Receptors (genetics, metabolism)
  • Protein Binding
  • RNA Interference
  • Response Elements
  • Signal Transduction
  • Sterol Regulatory Element Binding Protein 1 (genetics)
  • T-Lymphocytes (drug effects, ultrastructure)
  • Transcription, Genetic (drug effects)
  • Tumor Suppressor Proteins (genetics)
  • Withanolides (pharmacology)

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