Reduction of intersectin1-s induced apoptosis of human glioblastoma cells

Brain Res. 2010 Sep 10:1351:222-228. doi: 10.1016/j.brainres.2010.05.028. Epub 2010 May 21.

Abstract

Malignant gliomas have a high proliferation ability and high tendency to invade diffusely into surrounding healthy brain tissues, thereby precluding their successful surgical removal. Intersectin1 (also called ITSN1) as a molecular linker in the central nervous system is well known as an important regulator of endocytosis and exocytosis. ITSN1 has two isoforms: ITSN1-l and ITSN1-s. In this study, we show that siRNA-mediated down regulation of ITSN1-s induced glioma cells apoptosis. In addition, we demonstrate the possible mechanisms by which ITSN1-s functions in glioma cells apoptosis. Our data demonstrate that several key proteins, including FAK, Akt, Bcl-2, BAD which are critical for cells apoptosis were probably involved in ITSN1-s signaling pathways. Our results indicate that ITSN1-s is an effecter in regulation of gliomas cells apoptosis, and identify that ITSN1-s may be a new potentially anti-apoptosis target for therapeutic of gliomas.

Publication types

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

MeSH terms

  • Adaptor Proteins, Vesicular Transport / genetics
  • Adaptor Proteins, Vesicular Transport / physiology*
  • Animals
  • Apoptosis / genetics
  • Apoptosis / physiology*
  • Brain Neoplasms / genetics
  • Brain Neoplasms / metabolism*
  • Brain Neoplasms / pathology
  • Cell Line, Tumor
  • Down-Regulation / genetics
  • Down-Regulation / physiology*
  • Glioblastoma / genetics
  • Glioblastoma / metabolism*
  • Glioblastoma / pathology
  • Humans
  • Male
  • Mice
  • Mice, Nude
  • RNA, Small Interfering / genetics
  • Xenograft Model Antitumor Assays / methods

Substances

  • Adaptor Proteins, Vesicular Transport
  • ITSN1 protein, human
  • RNA, Small Interfering