RNAi-mediated silencing of leptin gene expression increases cell death in C6 glioblastoma cells

Brain Res Mol Brain Res. 2005 Oct 3;139(2):357-60. doi: 10.1016/j.molbrainres.2005.05.009.

Abstract

We previously demonstrated that the brain, pituitary, and C6 glioblastoma cells express leptin. To determine the physiological role of brain-derived leptin, we sought to selectively silence its expression using RNA interference (RNAi) in vitro. One of four potential targets, siRNA L7, reduced leptin mRNA by 50% (P < 0.05) and protein by 55% (P < 0.0001) in C6 cells. RNAi also induced a twofold increase in cell death as seen by ethidium homodimer-1 (P < 0.015) and TUNEL (P < 0.005) staining. These data suggest that endogenous leptin may be a critical factor promoting cell survival in the brain.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Cell Count
  • Cell Death / drug effects
  • Cell Line, Tumor
  • Dose-Response Relationship, Drug
  • Gene Expression Regulation / drug effects*
  • Gene Silencing / drug effects*
  • Glioblastoma / pathology
  • Glioblastoma / physiopathology
  • Leptin / genetics
  • Leptin / metabolism*
  • RNA Interference
  • RNA, Messenger / biosynthesis
  • RNA, Neoplasm / genetics
  • RNA, Neoplasm / metabolism
  • RNA, Small Interfering / pharmacology*
  • Rats
  • Reverse Transcriptase Polymerase Chain Reaction
  • Ribosomal Proteins / physiology
  • Time Factors

Substances

  • Leptin
  • RNA, Messenger
  • RNA, Neoplasm
  • RNA, Small Interfering
  • Ribosomal Proteins