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Resistance to TRAIL and how to surmount it
Danijela Maksimovic-Ivanic1, Stanislava Stosic-Grujicic, Ferdinando Nicoletti
1Department of Immunology, Institute for Biological Research Sinisa Stankovic, Belgrade University, Bulevar Despota Stefana 142, 11060 Belgrade, Serbia.
Immunologic Research
|March 13, 2012
Summary
Tumor cells resist TRAIL-induced toxicity through receptor changes or signaling issues. This review explores strategies to restore TRAIL sensitivity and enhance immune cell efficiency in cancer therapy.
Area of Science:
- Immunology
- Oncology
- Pharmacology
Background:
- Tumor cells develop resistance to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-induced toxicity as a survival mechanism.
- Resistance pathways include altered receptor expression (functional or decoy) and intracellular signaling defects.
- This resistance hinders effective anti-cancer immune responses.
Purpose of the Study:
- To review mechanisms by which tumor cells evade TRAIL-mediated apoptosis.
- To explore therapeutic strategies for overcoming TRAIL resistance.
- To suggest novel approaches for enhancing immune cell efficacy in cancer treatment.
Main Methods:
- Literature review of studies on TRAIL resistance mechanisms in cancer.
- Analysis of drug-induced sensitization to TRAIL (cytostatic and noncytostatic agents).
- Examination of intracellular and membrane-level signaling pathways involved in TRAIL resistance.
Main Results:
- Various drugs, including protease inhibitors and NO-hybridized molecules, can restore TRAIL sensitivity.
- Reconstitution of sensitivity involves modulating specific membrane and intracellular signals.
- Understanding these pathways is crucial for developing effective combination therapies.
Conclusions:
- Targeting resistance mechanisms can re-sensitize tumors to TRAIL-induced apoptosis.
- Novel strategies can reset immune cell efficiency for improved cancer treatment outcomes.
- Combination therapies hold promise for overcoming TRAIL resistance and enhancing anti-cancer immunity.
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