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Targeting p53 as a therapeutic strategy in sensitizing TRAIL-induced apoptosis in cancer cells

Jing Zhao1, Yixin Lu, Han-Ming Shen

  • 1Department of Epidemiology and Public Health, Yong Loo Lin School of Medicine, National University of Singapore, 16 Medical Drive, Singapore, Republic of Singapore.

Cancer Letters
|October 28, 2011
PubMed

Insights

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) shows promise for cancer therapy by inducing cancer cell death. Targeting the tumor suppressor p53 may overcome TRAIL resistance in cancers with functional p53.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induces apoptosis selectively in cancer cells.
  • Increasing TRAIL resistance in human cancer necessitates novel therapeutic strategies.
  • The tumor suppressor p53 plays a critical role in cellular stress responses.

Purpose of the Study:

  • To review the relationship between p53 and TRAIL-mediated apoptosis.
  • To summarize strategies targeting p53 to enhance TRAIL-induced apoptosis in cancer.

Main Methods:

  • Literature review of studies on TRAIL, p53, and cancer apoptosis.
  • Analysis of therapeutic approaches targeting the p53 pathway.
  • Synthesis of current understanding of p53's role in TRAIL resistance.

Main Results:

  • TRAIL induces apoptosis in cancer cells, but resistance is a significant challenge.
  • p53 is involved in cellular responses to stress and can influence TRAIL sensitivity.
  • Targeting p53 is a potential strategy to overcome TRAIL resistance in certain cancers.

Conclusions:

  • Restoring or activating p53 function may sensitize resistant cancer cells to TRAIL therapy.
  • Targeting p53 represents a promising approach for enhancing TRAIL efficacy in cancers with wild-type p53.
  • Further research into p53-TRAIL interactions is crucial for developing effective cancer treatments.

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