An RNAi screen identifies TRRAP as a regulator of brain tumor-initiating cell differentiation

Cell Stem Cell. 2010 Jan 8;6(1):37-47. doi: 10.1016/j.stem.2009.11.002.

Abstract

Glioblastoma multiforme (GBM) is a highly aggressive form of brain cancer associated with a very poor prognosis. Recently, the initiation and growth of GBM has been linked to brain tumor-initiating cells (BTICs), which are poorly differentiated and share features with neural stem cells (NSCs). Here we describe a kinome-wide RNA interference screen to identify factors that control the tumorigenicity of BTICs. We identified several genes whose silencing induces differentiation of BTICs derived from multiple GBM patients. In particular, knockdown of the adaptor protein TRRAP significantly increased differentiation of cultured BTICs, sensitized the cells to apoptotic stimuli, and negatively affected cell cycle progression. TRRAP knockdown also significantly suppressed tumor formation upon intracranial BTIC implantation into mice. Together, these findings support a critical role for TRRAP in maintaining a tumorigenic, stem cell-like state.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / analysis*
  • Adaptor Proteins, Signal Transducing / genetics
  • Animals
  • Apoptosis
  • Brain Neoplasms / chemistry*
  • Brain Neoplasms / genetics
  • Brain Neoplasms / pathology
  • Cell Differentiation*
  • Cell Transformation, Neoplastic / chemistry*
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / pathology
  • Female
  • Gene Expression Regulation, Neoplastic
  • Glioblastoma / chemistry*
  • Glioblastoma / genetics
  • Glioblastoma / pathology
  • Humans
  • Mice
  • Mice, SCID
  • Neoplastic Stem Cells / chemistry*
  • Neoplastic Stem Cells / cytology
  • Nuclear Proteins / analysis*
  • Nuclear Proteins / genetics
  • RNA Interference*
  • Tumor Cells, Cultured
  • Xenograft Model Antitumor Assays

Substances

  • Adaptor Proteins, Signal Transducing
  • Nuclear Proteins
  • transformation-transcription domain-associated protein