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Updated: Oct 9, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Caspase-dependent chemotherapy-induced death of glioma cells requires mitochondrial cytochrome c release

T Glaser1, M Weller

  • 1Laboratory of Molecular Neuro-Oncology, Department of Neurology, University of Tübingen, Tübingen, Germany.

Biochemical and Biophysical Research Communications
|February 22, 2001
PubMed

Insights

Chemotherapy triggers programmed cell death (apoptosis) in malignant glioma cells by activating caspases, primarily through the mitochondrial pathway. This cancer therapy approach targets essential cell death mechanisms.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Chemotherapy induces apoptosis in malignant glioma cells via death receptor-independent caspase activation.
  • Specific caspases beyond 3 and 8 are involved in this process.

Purpose of the Study:

  • To investigate the role of various caspases and the mitochondrial pathway in chemotherapy-induced apoptosis of human malignant glioma cells.
  • To determine the specific molecular targets of cytotoxic drugs in glioma apoptosis.

Main Methods:

  • Analysis of constitutive caspase expression in human malignant glioma cell lines.
  • Assessment of caspase activation, cytochrome c release, and cell death following cytotoxic drug treatment.
  • Utilizing caspase inhibitors (zVAD-fmk, crm-A) and BCL-X(L) to modulate apoptosis.

Main Results:

  • Caspases 1, 2, 3, 7, 8, and 9 are constitutively expressed in most glioma cell lines.
  • Drug-induced apoptosis involves delayed activation of caspases 2, 7, and 9, inhibited by zVAD-fmk.
  • Cytochrome c release from mitochondria precedes caspase activation and is prevented by BCL-X(L) expression.

Conclusions:

  • Cancer chemotherapy targets the mitochondrial, caspase-dependent pathway in human malignant glioma cells.
  • Mitochondrial integrity and caspase activation are critical for drug-induced glioma cell death.

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