| Pretreatment with paclitaxel enhances apo-2 ligand/tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis of prostate cancer cells by inducing death receptors 4 and 5 protein levels. | |
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MedLine Citation:
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PMID: 11212279 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We have demonstrated that Apo-2 ligand (Apo-2L)/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis of human prostate cancer PC-3, DU145, and LNCaP cells in a dose-dependent manner, with PC-3 cells displaying the greatest sensitivity to Apo-2L/TRAIL. Susceptibility of the prostate cancer cell types to Apo-2L/TRAIL-induced apoptosis did not appear to correlate with the levels of the Apo-2L/TRAIL receptors death receptor (DR) 4 (TRAIL receptor 1) or DR5 (TRAIL receptor 2), decoy receptor (DcR) 1 and DcR2, Flame-1, or the inhibitors of apoptosis proteins family of proteins. Apo-2L/TRAIL-induced apoptosis of PC-3 cells was associated with the processing of caspase-8, caspase-10, and the proapoptotic Bid protein, resulting in the cytosolic accumulation of cytochrome c as well as the processing of procaspase-9 and procaspase-3. Cotreatment with the caspase-8 inhibitor z-IETD-fmk or DR4:Fc significantly inhibited Apo-2L/TRAIL-induced apoptosis. Treatment with paclitaxel or taxotere increased DR4 and/or DR5 protein levels (up to 8-fold) without affecting the protein levels of DcR1 and DcR2, Apo-2L/TRAIL, Fas, or Fas ligand. Up-regulation of DR4 and DR5 was not preceded by the induction of their mRNA levels but was inhibited by cotreatment with cycloheximide. Importantly, sequential treatment of PC-3, DU145, and LNCaP cells with paclitaxel followed by Apo-2L/TRAIL induced significantly more apoptosis than Apo-2L/TRAIL treatment alone (P < 0.01). This was also associated with greater processing of procaspase-8 and Bid, as well as greater cytosolic accumulation of cytochrome c and the processing of caspase-3. These findings indicate that up-regulation of DR4 and DR5 protein levels by treatment with paclitaxel enhances subsequent Apo-2L/TRAIL-induced apoptosis of human prostate cancer cells. |
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Authors:
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R Nimmanapalli; C L Perkins; M Orlando; E O'Bryan; D Nguyen; K N Bhalla |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Cancer research Volume: 61 ISSN: 0008-5472 ISO Abbreviation: Cancer Res. Publication Date: 2001 Jan |
Date Detail:
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Created Date: 2001-02-09 Completed Date: 2001-02-22 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 2984705R Medline TA: Cancer Res Country: United States |
Other Details:
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Languages: eng Pagination: 759-63 Citation Subset: IM |
Affiliation:
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Moffitt Cancer Center and Research Institute, University of South Florida, Tampa 33612, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antineoplastic Agents, Phytogenic
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pharmacology Apoptosis / drug effects* Apoptosis Regulatory Proteins Blotting, Western Dose-Response Relationship, Drug Drug Synergism Humans Male Membrane Glycoproteins / pharmacology* Paclitaxel / pharmacology* Prostatic Neoplasms / metabolism, pathology, prevention & control* Receptors, TNF-Related Apoptosis-Inducing Ligand Receptors, Tumor Necrosis Factor / drug effects*, metabolism TNF-Related Apoptosis-Inducing Ligand Tumor Cells, Cultured Tumor Necrosis Factor-alpha / pharmacology* Up-Regulation / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Antineoplastic Agents, Phytogenic; 0/Apoptosis Regulatory Proteins; 0/Membrane Glycoproteins; 0/Receptors, TNF-Related Apoptosis-Inducing Ligand; 0/Receptors, Tumor Necrosis Factor; 0/TNF-Related Apoptosis-Inducing Ligand; 0/TNFRSF10A protein, human; 0/TNFRSF10B protein, human; 0/TNFSF10 protein, human; 0/Tumor Necrosis Factor-alpha; 33069-62-4/Paclitaxel |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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