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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.
Cancer Res. 2001 Jan 15; 61(2):759-63.CR

Abstract

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.

Authors+Show Affiliations

Nimmanapalli R
Moffitt Cancer Center and Research Institute, University of South Florida, Tampa 33612, USA.
Perkins CL
No affiliation info available
Orlando M
No affiliation info available
O'Bryan E
No affiliation info available
Nguyen D
No affiliation info available
Bhalla KN
No affiliation info available

MeSH

Antineoplastic Agents, PhytogenicApoptosisApoptosis Regulatory ProteinsBlotting, WesternDose-Response Relationship, DrugDrug SynergismHumansMaleMembrane GlycoproteinsPaclitaxelProstatic NeoplasmsReceptors, TNF-Related Apoptosis-Inducing LigandReceptors, Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandTumor Cells, CulturedTumor Necrosis Factor-alphaUp-Regulation

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11212279

Citation

Nimmanapalli, R, et al. "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." Cancer Research, vol. 61, no. 2, 2001, pp. 759-63.
Nimmanapalli R, Perkins CL, Orlando M, et al. 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. Cancer Res. 2001;61(2):759-63.
Nimmanapalli, R., Perkins, C. L., Orlando, M., O'Bryan, E., Nguyen, D., & Bhalla, K. N. (2001). 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. Cancer Research, 61(2), 759-63.
Nimmanapalli R, et al. 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. Cancer Res. 2001 Jan 15;61(2):759-63. PubMed PMID: 11212279.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Nimmanapalli,R, AU - Perkins,C L, AU - Orlando,M, AU - O'Bryan,E, AU - Nguyen,D, AU - Bhalla,K N, PY - 2001/2/24/pubmed PY - 2001/3/3/medline PY - 2001/2/24/entrez SP - 759 EP - 63 JF - Cancer research JO - Cancer Res VL - 61 IS - 2 N2 - 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. SN - 0008-5472 UR - https://www.unboundmedicine.com/medline/citation/11212279/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_ DB - PRIME DP - Unbound Medicine ER -
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