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Related Experiment Videos

Apoptosis and drug response.

J A Houghton1

  • 1Department of Molecular Pharmacology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.

Current Opinion in Oncology
|November 5, 1999
PubMed
Summary

Drug-induced DNA damage triggers apoptosis via p53 and transcription factors activating FasL. Understanding these pathways, including death receptors, is crucial for cancer treatment responses.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • p53 plays a critical role in apoptosis following DNA damage.
  • Transcription factors like NF-kappaB and AP-1 are involved in drug-induced apoptosis.
  • Death receptors (Fas, DR4, DR5) and their ligands (FasL, TRAIL) are key in cancer cell death.

Purpose of the Study:

  • To further define the role of p53 and its associated signaling pathways in apoptosis after drug-induced DNA damage.
  • To investigate the activation of transcription factors NF-kappaB and AP-1 and their role in FasL transactivation.
  • To explore the significance of death receptors (Fas, DR4, DR5) in drug-induced apoptosis in human cancers.

Main Methods:

  • Analysis of p53 signaling pathways.
  • Investigation of transcription factor activation (NF-kappaB, AP-1).
  • Study of FasL transactivation and death receptor signaling.

Main Results:

  • p53 and signaling events upstream and downstream of p53 are critical in drug-induced apoptosis.
  • NF-kappaB and AP-1 are activated by chemotherapeutic agents and transactivate FasL.
  • Death receptors Fas, DR4, and DR5 mediate caspase activation and apoptosis in response to FasL and TRAIL.

Conclusions:

  • Apoptosis is a primary mechanism of drug-induced cell death in preclinical models and sensitive tumors.
  • Drug-induced cell death encompasses apoptosis, necrosis, and mitotic death, requiring further in vivo delineation.
  • Understanding these molecular pathways is essential for optimizing cancer therapy.

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