Cristazine, a novel dioxopiperazine alkaloid, induces apoptosis via the death receptor pathway in A431 cells

2019 ◽  
Vol 80 (4) ◽  
pp. 504-512 ◽  
Author(s):  
Mi Jeong Jo ◽  
Maheshkumar P. Patil ◽  
Hyun Il Jung ◽  
Yong Bae Seo ◽  
Han Kyu Lim ◽  
...  
Keyword(s):  
Death Receptor ◽  
A431 Cells ◽  
Death Receptor Pathway

Lead induces apoptosis in mouse TM3 Leydig cells through the Fas/FasL death receptor pathway

2017 ◽  
Vol 56 ◽  
pp. 99-105 ◽  
Author(s):  
Xiuyuan He ◽  
Jing Wu ◽  
Liyun Yuan ◽  
Feng Lin ◽  
Jine Yi ◽  
...  
Keyword(s):  
Leydig Cells ◽  
Death Receptor ◽  
Death Receptor Pathway

The Protective Role of Selenium Against AFB1-Induced Liver Apoptosis by Death Receptor Pathway in Broilers

2019 ◽  
Vol 191 (2) ◽  
pp. 453-463 ◽  
Author(s):  
Bangyuan Wu ◽  
Muhammad Jameel Mughal ◽  
Jing Fang ◽  
Xi Peng
Keyword(s):  
Death Receptor ◽  
Protective Role ◽  
Death Receptor Pathway

Comparative cytotoxicity and apoptotic pathways induced by nanosilver in human liver HepG2 and L02 cells

2018 ◽  
Vol 37 (12) ◽  
pp. 1293-1309 ◽  
Author(s):  
Y Xue ◽  
J Wang ◽  
Y Huang ◽  
X Gao ◽  
L Kong ◽  
...  
Keyword(s):  
Cell Line ◽  
Hepg2 Cells ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Hepatoma Cell ◽  
Death Receptor ◽  
Hepatoma Cell Line ◽  
Dependent Manner ◽  
Death Receptor Pathway ◽  
L02 Cells

Silver nanoparticles are used in many commercial products in daily life. Exposure to nanosilver has hepatotoxic effects in animals. This study investigated the cytotoxicity associated with polyvinylpyrrolidone-coated nanosilver (23.44 ± 4.92 nm in diameter) exposure in the human hepatoma cell line (HepG2) and normal hepatic cell line (L02), and the molecular mechanisms induced by nanosilver in HepG2 cells. Nanosilver, in doses of 20–160 μg mL−1 for 24 and 48 h, reduced cell viability in a dose- and time-dependent manner and induced cell membrane leakage and mitochondria injury in both cell lines; these effects were more pronounced in HepG2 cells than in L02 cells. Intracellular oxidative stress was documented by reactive oxygen species (ROS) being generated in HepG2 cells but not in L02 cells, an effect possibly due to differential uptake of nanosilver by cancer cells and normal cells. In HepG2 cells, apoptosis was documented by finding that ROS triggered a decrease in mitochondrial membrane potential, an increase in cytochrome c release, activation of caspase 3 and caspase 9, and a decrease in the ratio of Bcl-2/Bax. Furthermore, nanosilver activated the Fas death receptor pathway by downregulation of nuclear factor-κB and activation of caspase 8 and caspase 3. These results suggest that apoptosis induced by nanosilver in HepG2 cells is mediated via a mitochondria-dependent pathway and the Fas death receptor pathway. These findings provide toxicological and mechanistic information that can help in assessing the effects of nanosilver in biological systems, including the potential for anticancer activities.

scholarly journals Differential activation of the death receptor pathway in human target cells induced by cytotoxic T lymphocytes showing different kinetics of killing

Haematologica ◽  
2007 ◽  
Vol 92 (12) ◽  
pp. 1671-1678 ◽  
Author(s):  
J. F. de Vries ◽  
P. A. von dem Borne ◽  
S. A.P. van Luxemburg-Heijs ◽  
M. H.M. Heemskerk ◽  
R. Willemze ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Death Receptor ◽  
Target Cells ◽  
Differential Activation ◽  
Death Receptor Pathway ◽  
Kinetics Of

scholarly journals Molecular Determinants of the Caspase-promoting Activity of Smac/DIABLO and Its Role in the Death Receptor Pathway

2000 ◽  
Vol 275 (46) ◽  
pp. 36152-36157 ◽  
Author(s):  
Srinivasa M. Srinivasula ◽  
Pinaki Datta ◽  
Xue-Jun Fan ◽  
Teresa Fernandes-Alnemri ◽  
Ziwei Huang ◽  
...  
Keyword(s):  
Death Receptor ◽  
Death Receptor Pathway ◽  
Molecular Determinants

Inhibitors of histone deacetylases induce tumor-selective apoptosis through activation of the death receptor pathway

2004 ◽  
Vol 11 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Alessandra Insinga ◽  
Silvia Monestiroli ◽  
Simona Ronzoni ◽  
Vania Gelmetti ◽  
Francesco Marchesi ◽  
...  
Keyword(s):  
Histone Deacetylases ◽  
Death Receptor ◽  
Death Receptor Pathway ◽  
Tumor Selective

scholarly journals Inhibition of the Death Receptor Pathway by cFLIP Confers Partial Engraftment of MHC Class I-Deficient Stem Cells and Reduces Tumor Clearance in Perforin-Deficient Mice

2001 ◽  
Vol 167 (8) ◽  
pp. 4230-4237 ◽  
Author(s):  
Mesha Austin Taylor ◽  
Preet M. Chaudhary ◽  
Jennifer Klem ◽  
Vinay Kumar ◽  
John D. Schatzle ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mhc Class I ◽  
Death Receptor ◽  
Class I ◽  
Death Receptor Pathway ◽  
Tumor Clearance ◽  
Deficient Mice

scholarly journals Differential expression of apoptosis-related genes from death receptor pathway in chronic myeloproliferative diseases

2010 ◽  
Vol 64 (1) ◽  
pp. 75-82 ◽  
Author(s):  
R. Tognon ◽  
E. P. L. Gasparotto ◽  
J. M. G. Leroy ◽  
G. L. V. Oliveira ◽  
R. P. Neves ◽  
...  
Keyword(s):  
Differential Expression ◽  
Death Receptor ◽  
Death Receptor Pathway ◽  
Myeloproliferative Diseases ◽  
Chronic Myeloproliferative Diseases

Study on Apoptosis of Human Promyelocytic Leukemia HL-60 Cells Induced by Fucosterol via Death Receptor Pathway

2013 ◽  
Vol 790 ◽  
pp. 607-610 ◽  
Author(s):  
Yu Bin Ji ◽  
Dong Xue Song ◽  
Chen Feng Ji
Keyword(s):  
Laser Scanning ◽  
Caspase 3 ◽  
Death Receptor ◽  
Promyelocytic Leukemia ◽  
Caspase 8 ◽  
Laser Scanning Confocal Microscope ◽  
Death Receptor Pathway ◽  
Mtt Method ◽  
Induction Of Apoptosis ◽  
Anti Tumor Activity

The purpose of this study is to investigate the effect of fucosterol on the induction of apoptosis and the molecular mechanism involved in Human promyelocytic leukemia HL-60 Cells. HL-60 Cells were treated with different concentrations of fucosterol at different time. MTT method was used to study fucosterol anti-tumor activity. Morphology observation was performed to determine the effects of fucosterol on apoptosis of HL-60 cells. Flow cytometry (FCM) was used to detect the cell cycle. Laser scanning confocal microscope (LSCM) was used to analyze the expressions of Fas, FasL, Fadd and Caspase-8. Caspase activity kits were used to determine the activity of Caspase-8 and Caspase-3. The results showed fucosterol could inhibit the growth of HL-60 cells, and the apoptosis morphology for 48 h treatment was obvious, which showed cell protuberance, cytoplasm concentrated and apoptotic body. Fucosterol treatment for 24 h increased the protein expression of Fas, FasL, Fadd and Caspase-8. It also showed that the activity of Caspase-3 and Caspase-8 has increased significantly. In conclusion, Fucosterol could induce HL-60 cells apoptosis via death receptor pathway.

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