Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/6672
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DC Field | Value | Language |
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dc.contributor.author | Bouralexis, S. | - |
dc.contributor.author | Findlay, D. | - |
dc.contributor.author | Atkins, G. | - |
dc.contributor.author | Labrinidis, A. | - |
dc.contributor.author | Hay, S. | - |
dc.contributor.author | Evdokiou, A. | - |
dc.date.issued | 2003 | - |
dc.identifier.citation | British Journal of Cancer, 2003; 89(1):206-214 | - |
dc.identifier.issn | 0007-0920 | - |
dc.identifier.issn | 1532-1827 | - |
dc.identifier.uri | http://hdl.handle.net/2440/6672 | - |
dc.description | © 2003 Cancer Research UK | - |
dc.description.abstract | Apo2 ligand (Apo2L, also known as TRAIL) is a member of the tumour necrosis factor (TNF) family of cytokines that selectively induces the death of cancer cells, but not of normal cells. We observed that recombinant Apo2L/TRAIL was proapoptotic in early-passage BTK-143 osteogenic sarcoma cells, inducing 80% cell death during a 24 h treatment period. Apo2L/TRAIL-induced apoptosis was blocked by caspase inhibition. With increasing passage in culture, BTK-143 cells became progressively resistant to the apoptotic effects of Apo2L/TRAIL . RNA and flow cytometric analysis demonstrated that resistance to Apo2L/TRAIL was paralleled by progressive acquisition of the decoy receptor, DcR2. Blocking of DcR2 function with a specific anti-DcR2 antibody restored sensitivity to Apo2L/TRAIL in a dose-dependent manner. Importantly, treatment of resistant cells with the chemotherapeutic agents doxorubicin, cisplatin and etoposide reversed the resistance to Apo2L/TRAIL, which was associated with drug-induced upregulation of mRNA encoding the death receptors DR4 and DR5. BTK-143 cells thus represent a useful model system to investigate both the mechanisms of acquisition of resistance of tumour cells to Apo2L/TRAIL and the use of conventional drugs and novel agents to overcome resistance to Apo2L/TRAIL. | - |
dc.description.statementofresponsibility | S Bouralexis, D M Findlay, G J Atkins, A Labrinidis, S Hay & A Evdokiou | - |
dc.language.iso | en | - |
dc.publisher | Churchill Livingstone | - |
dc.source.uri | http://dx.doi.org/10.1038/sj.bjc.6601021 | - |
dc.subject | DcR2 | - |
dc.subject | Apo2L/TRAIL | - |
dc.subject | osteosarcoma | - |
dc.subject | resistance | - |
dc.subject | chemotherapy | - |
dc.subject | apoptosis | - |
dc.title | Progressive resistance of BTK-143 osteosarcoma cells to Apo2L/TRAIL-induced apoptosis is mediated by acquisition of DcR2/TRAIL-R4 expression: resensitisation with chemotherapy | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1038/sj.bjc.6601021 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Atkins, G. [0000-0002-3123-9861] | - |
dc.identifier.orcid | Evdokiou, A. [0000-0001-8321-9806] | - |
Appears in Collections: | Aurora harvest 5 Orthopaedics and Trauma publications |
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hdl_6672.pdf | Published version | 221.64 kB | Adobe PDF | View/Open |
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