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Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies

Giuseppa Pistritto1, Daniela Trisciuoglio2, Claudia Ceci1

  • 1Department of Systems Medicine, University "Tor Vergata", 00133 Rome, Italy.

Aging
|March 29, 2016
PubMed

Insights

Apoptosis, or programmed cell death, is crucial for removing damaged cells. Its dysregulation fuels cancer development and therapy resistance, highlighting the need for targeted apoptosis modulation strategies.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Apoptosis (programmed cell death) removes damaged cells via internal or external signals.
  • Dysregulation of apoptosis is a key factor in cancer development, progression, and therapeutic resistance.
  • Current cancer therapies often rely on intact apoptotic pathways for efficacy.

Purpose of the Study:

  • To review the fundamental regulators of apoptosis.
  • To explore how deregulation of apoptosis contributes to cancer cell resistance to therapies.
  • To briefly discuss therapeutic strategies targeting apoptosis.

Main Methods:

  • Literature review focusing on apoptosis regulators and their role in cancer.
  • Analysis of how anti-apoptotic (e.g., Bcl-2, Bcl-xL) and pro-apoptotic (e.g., p53) factors influence therapy resistance.
  • Overview of therapeutic approaches modulating apoptotic activity.

Main Results:

  • Activation of anti-apoptotic factors and inactivation of pro-apoptotic factors lead to cancer cell resistance.
  • Defects in apoptotic pathways limit the efficacy of conventional anticancer drugs.
  • Understanding apoptosis signaling is vital for overcoming drug resistance.

Conclusions:

  • Targeting apoptotic pathways offers potential for improving cancer therapy efficacy.
  • Modulating apoptosis regulators can help bypass or overcome therapeutic resistance.
  • Further research into apoptosis mechanisms is crucial for advancing cancer treatment.
Keywords:
apoptosiscancerdefective apoptotic pathwaysmiRNAsp53small molecules

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