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Updated: Jul 2, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
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.
Abstract:
The major limitation of conventional chemotherapy drugs is their lack of specificity for cancer cells. As a selective apoptosis-inducing agent, tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has emerged as an attractive alternative. However, most of the cancer cells are found to be either intrinsically resistant to the TRAIL protein or may develop resistance after multiple treatments, and TRAIL resistance can induce epithelial-to-mesenchymal transition (EMT) at a later stage, promoting cancer invasion and migration. Interestingly, E-cadherin loss has been linked to TRAIL resistance and initiation of EMT, making E-cadherin re-expression a potential target to overcome these obstacles. Recent research suggests that re-expressing E-cadherin may reduce TRAIL resistance by enhancing TRAIL-induced apoptosis and preventing EMT by modulating EMT signalling factors. This reversal of EMT, can also aid in improving TRAIL-induced apoptosis. Therefore, this review provides remarkable insights into the mechanisms underlying E-cadherin re-expression, clinical implications, and potentiation, as well as the research gaps of E-cadherin re-expression in the current cancer treatment.
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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