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Autophagy as a mechanism of Apo2L/TRAIL resistance

Arishya Sharma1, Alexandru Almasan1,2

  • 1a Department of Cancer Biology , Lerner Research Institute , Cleveland , OH , USA.

Cancer Biology & Therapy
|August 2, 2018
PubMed

Insights

Apo2L/TRAIL therapy shows promise for cancer but faces drug resistance. Targeting autophagy, a cellular process, may overcome this resistance by influencing cancer cell survival or death in response to Apo2L/TRAIL.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Apo2L/TRAIL selectively induces apoptosis in tumor cells, offering therapeutic potential.
  • Drug resistance remains a significant challenge in Apo2L/TRAIL therapy.
  • Autophagy is consistently activated by apoptosis-inducing stimuli like Apo2L/TRAIL.

Purpose of the Study:

  • To review the interplay between autophagy and apoptosis in cancer cells treated with Apo2L/TRAIL.
  • To explore how autophagy modulation can overcome Apo2L/TRAIL resistance.
  • To understand the role of autophagic flux in determining cancer cell fate.

Main Methods:

  • Literature review of studies investigating Apo2L/TRAIL therapy and autophagy.
  • Analysis of molecular mechanisms linking autophagy and apoptosis.
  • Examination of factors influencing autophagic flux in cancer cells.

Main Results:

  • Autophagy's role in Apo2L/TRAIL response is context-dependent, potentially leading to cell survival or death.
  • Intact autophagic flux may be crucial for mediating cell death in response to Apo2L/TRAIL.
  • Dysregulated autophagy can contribute to resistance against Apo2L/TRAIL therapy.

Conclusions:

  • Targeting autophagy presents a promising strategy to enhance Apo2L/TRAIL efficacy.
  • Understanding the balance between autophagy and apoptosis is key to overcoming drug resistance.
  • Further research into modulating autophagy could lead to improved cancer treatment outcomes.
Keywords:
Apo2L/TRAILApoptosisautophagosomeautophagyfluxp62/SQSTM1prostate cancer

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