E-cadherin re-expression: Its potential in combating TRAIL resistance and reversing epithelial-to-mesenchymal

Ser Hui San1, Siew Ching Ngai1

  • 1School of Biosciences, Faculty of Science and Engineering, University of Nottingham Malaysia, 43500 Semenyih, Selangor, Malaysia.

Gene
|February 19, 2024
PubMed

Insights

Re-expressing E-cadherin can overcome cancer cell resistance to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) therapy. This strategy enhances TRAIL-induced apoptosis and prevents cancer cell invasion by reversing epithelial-to-mesenchymal transition (EMT).

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Conventional chemotherapy lacks cancer cell specificity.
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) offers selective cancer cell apoptosis induction.
  • TRAIL resistance and epithelial-to-mesenchymal transition (EMT) promote cancer invasion and migration.

Purpose of the Study:

  • To review mechanisms of E-cadherin re-expression for overcoming TRAIL resistance.
  • To explore clinical implications and potentiation strategies for E-cadherin re-expression.
  • To identify research gaps in using E-cadherin re-expression for cancer treatment.

Main Methods:

  • Review of current literature on TRAIL resistance and EMT.
  • Analysis of studies investigating E-cadherin re-expression.
  • Evaluation of E-cadherin's role in modulating apoptosis and EMT signaling.

Main Results:

  • E-cadherin loss is linked to TRAIL resistance and EMT initiation.
  • E-cadherin re-expression enhances TRAIL-induced apoptosis.
  • Re-expressing E-cadherin prevents EMT and reverses its pro-invasive effects.

Conclusions:

  • E-cadherin re-expression is a promising strategy to overcome TRAIL resistance in cancer.
  • Targeting E-cadherin can improve TRAIL efficacy and reduce cancer metastasis.
  • Further research is needed to fully leverage E-cadherin re-expression in clinical settings.

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