Therapeutic exploitation of apoptosis and autophagy for glioblastoma

Donat Kögel*, Simone Fulda, Michel Mittelbronn

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

52 Citations (Scopus)

Abstract

Induction of caspase-dependent apoptosis (type I cell death) is a major mechanism by which most chemotherapeutic drugs and radiation kill tumor cells. However conventional cancer therapies fail to mediate their effects in a target-specific fashion. The extremely unfavorable prognosis for patients suffering from glioblastomas (GBMs) is strongly correlated to the intrinsic apoptosis resistance of GBM cells which especially occurs in diffusely migrating tumor cells. The ultimate goal for molecular apoptosis-based therapies is to target specific components of the two major apoptotic pathways i.e. the extrinsic and the intrinsic pathway to trigger tumor-selective apoptosis while at the same time limiting toxicity in normal tissues. Induction of autophagic cell death (type II cell death) by proautophagic drugs is an alternative and emerging concept to trigger glioma cell death and to exploit caspase-independent programmed cell death pathways for the development of novel glioma therapies. This review provides an up to date and comprehensive report on the relevant pre-clinical and clinical drugs interfering with the major apoptosis and autophagy pathways their therapeutic potential in glioma and adresses potential future perspectives in this exciting field of research.

Original languageEnglish
Pages (from-to)438-449
Number of pages12
JournalAnti-Cancer Agents in Medicinal Chemistry
Volume10
Issue number6
DOIs
Publication statusPublished - 2010
Externally publishedYes

Keywords

  • Akt
  • Apoptosis
  • Autophagy
  • Bcl-2
  • Beclin1
  • Caspase
  • Death receptor
  • Inhibitor of apoptosis
  • Lysosomal protease
  • MTOR

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