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Cilengitide induces autophagy-mediated cell death in glioma cells

  • Stephanie L. Lomonaco
  • , Susan Finniss
  • , Cunli Xiang
  • , Hae Kyung Lee
  • , Wei Jiang
  • , Nancy Lemke
  • , Sandra A. Rempel
  • , Tom Mikkelsen
  • , Chaya Brodie
  • Henry Ford Health System

Research output: Contribution to journalArticlepeer-review

43 Scopus citations

Abstract

We studied the effect of the integrin inhibitor cilengitide in glioma cells. Cilengitide induced cell detachment and decreased cell viability, and induction of autophagy followed by cell apoptosis. In addition, cilengitide decreased the cell renewal of glioma stem-like cells (GSCs). Inhibition of autophagy decreased the cytotoxic effect of cilengitide. Pretreatment of glioma cells and GSCs with cilengitide prior to γ-irradiation resulted in a larger increase in autophagy and a more significant decrease in cell survival. We found that cilengitide induced autophagy collectively in glioma cells, xenografts, and GSCs, which contributed to its cytotoxic effects and sensitized these cells to γ-radiation.

Original languageEnglish
Pages (from-to)857-865
Number of pages9
JournalNeuro-Oncology
Volume13
Issue number8
DOIs
StatePublished - Aug 2011

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Autophagy
  • Beclin-1
  • Cilengitide
  • Glioma cells
  • Radiation

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