ArticleBritish journal of cancer2010
Fenretinide-dependent upregulation of death receptors through ASK1 and p38α enhances death receptor ligand-induced cell death in Ewing's sarcoma family of tumours.
Article in British journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 24 citations in OpenAlex.
- Cytotoxic and Cytostatic Effects of Nanoformulated Fenretinide on MG63 Osteosarcoma Cells.Pharmaceutics · 2026Article
- CD271 activation prevents low to high-risk progression of cutaneous squamous cell carcinoma and improves therapy outcomes.Journal of experimental & clinical cancer research : CR · 2023Article
- Targeting incretin hormones and the ASK-1 pathway as therapeutic options in the treatment of non-alcoholic steatohepatitis.Hepatology international · 2018Review
- Apoptosis signal-regulating kinase 1 mediates the inhibitory effect of hepatocyte nuclear factor-4α on hepatocellular carcinoma.Oncotarget · 2016Article
- The alkyllysophospholipid edelfosine enhances TRAIL-mediated apoptosis in gastric cancer cells through death receptor 5 and the mitochondrial pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Induction of Expression of p75 Neurotrophin Receptor Intracellular Domain Does Not Induce Expression or Enhance Activity of Mitochondrial Complex II.Oxidative medicine and cellular longevity · 2016Article
- Proliferation index: a continuous model to predict prognosis in patients with tumours of the Ewing's sarcoma family.PloS one · 2014Article
- Combination of fenretinide and selenite inhibits proliferation and induces apoptosis in ovarian cancer cells.International journal of molecular sciences · 2013Article
- Fenretinide sensitizes multidrug-resistant human neuroblastoma cells to antibody-independent and ch14.18-mediated NK cell cytotoxicity.Journal of molecular medicine (Berlin, Germany) · 2013Article
- Cell-based small-molecule compound screen identifies fenretinide as potential therapeutic for translocation-positive rhabdomyosarcoma.PloS one · 2013Article
- An essential role for p38 MAPK in cerebellar granule neuron precursor proliferation.Acta neuropathologica · 2012Article
- TRAIL receptor signaling and therapeutic option in bone tumors: the trap of the bone microenvironment.American journal of cancer research · 2012Article
- Heterogeneous role of the glutathione antioxidant system in modulating the response of ESFT to fenretinide in normoxia and hypoxia.PloS one · 2011Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundSustained p38(MAPK) phosphorylation upregulates p75 neurotrophin (p75(NTR)) and induces apoptosis in Ewing's sarcoma family of tumours (ESFT). As fenretinide induces ESFT death through sustained p38(MAPK) phosphorylation, we hypothesised that this may be effected through upregulation of death receptors (DRs) and that treatment of fenretinide plus DR ligands may enhance apoptosis.
methodsDR expression was determined by flow cytometry. Trypan blue exclusion assays, caspase-8 flow cytometry and immunoblotting for Bid were used to measure cell death.
resultsFenretinide upregulated cell surface expression of tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors, FAS and p75(NTR), in an ASK1- and p38α-dependent manner. Cotreatment with fenretinide and DR ligands resulted in synergistic death compared with either agent alone; caspase-8 and Bid were cleaved in a time-dependent manner. Fenretinide did not increase DR expression in non-malignant cells. Furthermore, fenretinide, TRAIL or a combination of both agents was non-cytotoxic to non-malignant cells. Etoposide and actinomycin D increased expression of all DRs examined, whereas vincristine increased FAS alone. Only actinomycin D and TRAIL, and etoposide with TRAIL or FasL, enhanced death compared with either agent alone.
conclusionThe synergistic death observed with fenretinide and DR ligands suggests that this combination may be an attractive strategy for the treatment of ESFT.
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