ArticleBritish journal of cancer2006
TRAIL sensitisation by arsenic trioxide is caspase-8 dependent and involves modulation of death receptor components and Akt.
Article in British journal of cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 34 citations in OpenAlex.
- Synergistic Enhancement of Apo2L/TRAIL and DR4-Induced Apoptosis by Arsenic Trioxide in Triple-Negative Breast Cancer Cells: A Comparison to Conventional Chemotherapy.Cell biochemistry and biophysics · 2025Article
- Sevelamer arsenite nanoparticle as a Pi-responsive drug carrier and embolic agent for chemoembolization.Drug delivery · 2022Article
- Article
- Piperlongumine and immune cytokine TRAIL synergize to promote tumor death.Scientific reports · 2015Article
- Arsenic trioxide reduces chemo-resistance to 5-fluorouracil and cisplatin in HBx-HepG2 cells via complex mechanisms.Cancer cell international · 2015Article
- Association of overexpression of hexokinase II with chemoresistance in epithelial ovarian cancer.Clinical and experimental medicine · 2014Article
- Kinetics in signal transduction pathways involving promiscuous oligomerizing receptors can be determined by receptor specificity: apoptosis induction by TRAIL.Molecular & cellular proteomics : MCP · 2012Article
- Differential activation of JNK1 isoforms by TRAIL receptors modulate apoptosis of colon cancer cell lines.British journal of cancer · 2009Article
- TRAIL in cancer therapy: present and future challenges.Expert opinion on therapeutic targets · 2007Review
- Sodium arsenite accelerates TRAIL-mediated apoptosis in melanoma cells through upregulation of TRAIL-R1/R2 surface levels and downregulation of cFLIP expression.Experimental cell research · 2006Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The majority of leukaemic cells are resistant to apoptosis induced by tumour necrosis factor-related apoptosis-inducing ligand (TRAIL). Here, we show that sublethal concentrations of arsenic trioxide (ATO) specifically enhanced TRAIL-induced apoptosis in leukaemic but not in other tumour cell lines. The combination of ATO and TRAIL synergistically enhanced cleavage of caspase-8, which was blocked by the caspase inhibitor IETD.fmk as well as in cells deficient for caspase-8, suggesting a requirement for the death-inducing signalling complex. Arsenic trioxide led to increased cell surface expression of DR5 (death receptor 5), inhibition of the serine/threonine kinase Akt and downregulation of the short isoform of FLIP (FLICE-inhibitory protein, FLIPS). Inhibition of the phosphatidylinositol 3 kinase (PI3K) was equally efficient in sensitising leukaemic cells to TRAIL with similar effects on DR5 and FLIPS expression, suggesting that ATO may in part act through inhibition of the PI3K/Akt signalling pathway. These results indicate that the enhancement in TRAIL-mediated apoptosis induced by ATO is due to alteration in the levels of multiple components and regulators of the death receptor-mediated pathway. These findings offer a promising and novel strategy involving a combination of TRAIL and ATO, or more specific Akt inhibitors in the treatment of various haematopoietic malignancies.
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