Exploring the TRAILs less travelled: TRAIL in cancer biology and therapy
Abstract
The discovery that the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis of cancer cells without causing toxicity in mice has led to the in-depth study of pro-apoptotic TRAIL receptor (TRAIL-R) signalling and the development of biotherapeutic drug candidates that activate TRAIL-Rs. The outcome of clinical trials with these TRAIL-R agonists has, however, been disappointing so far. Recent evidence indicates that many cancers, in addition to being TRAIL resistant, use the endogenous TRAIL-TRAIL-R system to their own advantage. However, novel insight on two fronts - how resistance of cancer cells to TRAIL-based pro-apoptotic therapies might be overcome, and how the pro-tumorigenic effects of endogenous TRAIL might be countered - gives reasonable hope that the TRAIL system can be harnessed to treat cancer. In this Review we assess the status quo of our understanding of the biology of the TRAIL-TRAIL-R system - as well as the gaps therein - and discuss the opportunities and challenges in effectively targeting this pathway.
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Death receptors include FAS, TNFRSF1A, TNFRSF10A, and TNFRSF10B.
“Death receptors include (but are not limited to): Fas cell surface death receptor (FAS; also known as CD95 or APO-1), and TNF receptor superfamily member 1A (TNFRSF1A; best known as TNFR1), 10a (TNFRSF10A; best known as TRAILR1 or DR4), and 10b (TNFRSF10B; best known as TRAILR2 or DR5) [269, 270, 272, 273].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [272]
Ability of some death receptors including TNFR1 to promote NF-κB activation over CASP8 activation depends on degree of receptor oligomerization, scaffolding functions of CASP8, and assembly of TNFR1-like complexes containing RIPK1 and LUBAC.
“The ability of some death receptors including TNFR1 to promote NF-κB activation over CASP8 activation appears to depend on the degree of receptor oligomerization (i.e., trimerization vs. higher-order multimerization) [343], the scaffolding (i.e., non-enzymatic) functions of CASP8, and the consequent assembly of TNFR1-like complexes containing RIPK1 and LUBAC [272, 286, 344].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [272]
Death receptor signaling can also lead to NF-κB activation, generally resulting in cell survival associated with robust inflammatory response.
“Death receptor signaling can also lead to NF-κB activation, generally resulting in cell survival associated with a robust inflammatory response [272, 342].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [272]
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Flagged first, then by citations
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Self-citationPhototherapy in cancer treatment: strategies and challenges
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- Authors
- von Karstedt, S., Montinaro, A., & Walczak, H.
- Affiliations
- University College London (GB)
- Corresponding author
- Walczak, Henning
- Venue
- Nature Reviews Cancer
- Published
- 2017-05-24
- Volume
- 17
- Issue
- 6
- Pages
- 352-366
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2620490360
- Cited by
- 556
- References
- 188
- Citations by year
- 2026: 27 · 2025: 48 · 2024: 58 · 2023: 77 · 2022: 63 · 2021: 84 · 2020: 73 · 2019: 64 · 2018: 47 · 2017: 14
- FWCI
- 5.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Wellcome Trust (096831/Z/11/Z)
- Cancer Research UK (515818, A17341, 522434, 525877)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Complementary and alternative medicine › Natural Compounds in Disease Treatment
- Keywords
- TRAIL, TRAIL receptors, apoptosis, TRAIL resistance, cancer therapy, tumor necrosis factor-related apoptosis-inducing ligand, clinical trial failure
- MeSH terms
- Humans, Neoplasms, Signal Transduction, Receptors, TNF-Related Apoptosis-Inducing Ligand, TNF-Related Apoptosis-Inducing Ligand
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