Murine hypodense eosinophils induce tumour cell apoptosis by a granzyme B-dependent mechanism

2001 ◽  
Vol 50 (6) ◽  
pp. 293-299 ◽  
Author(s):  
Darren James Costain ◽  
Ashim K. Guha ◽  
Robert Stefan Liwski ◽  
Timothy D. G. Lee
Keyword(s):  
Tumour Cell ◽  
Cell Apoptosis ◽  
Granzyme B ◽  
Dependent Mechanism

scholarly journals Nuclear translocation of granzyme B in target cell apoptosis

2000 ◽  
Vol 7 (1) ◽  
pp. 17-24 ◽  
Author(s):  
M J Pinkoski ◽  
J A Heibein ◽  
M Barry ◽  
R C Bleackley
Keyword(s):  
Target Cell ◽  
Cell Apoptosis ◽  
Nuclear Translocation ◽  
Granzyme B

scholarly journals Residual active granzyme B in cathepsin C–null lymphocytes is sufficient for perforin-dependent target cell apoptosis

2007 ◽  
Vol 204 (2) ◽  
pp. i3-i3
Author(s):  
Vivien R. Sutton ◽  
Nigel J. Waterhouse ◽  
Kylie A. Browne ◽  
Karin Sedelies ◽  
Annette Ciccone ◽  
...  
Keyword(s):  
Target Cell ◽  
Cell Apoptosis ◽  
Granzyme B ◽  
Cathepsin C

scholarly journals Role of peroxide and superoxide anion during tumour cell apoptosis

FEBS Letters ◽  
1997 ◽  
Vol 404 (1) ◽  
pp. 27-33 ◽  
Author(s):  
Adrienne Gorman ◽  
Adrian McGowan ◽  
Thomas G. Cotter
Keyword(s):  
Tumour Cell ◽  
Cell Apoptosis ◽  
Superoxide Anion

scholarly journals Invasive Trophoblasts Stimulate Vascular Smooth Muscle Cell Apoptosis by a Fas Ligand-Dependent Mechanism

2006 ◽  
Vol 169 (5) ◽  
pp. 1863-1874 ◽  
Author(s):  
Lynda K. Harris ◽  
Rosemary J. Keogh ◽  
Mark Wareing ◽  
Philip N. Baker ◽  
Judith E. Cartwright ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Apoptosis ◽  
Fas Ligand ◽  
Muscle Cell Apoptosis ◽  
Dependent Mechanism

scholarly journals Platelets are recruited to hepatocellular carcinoma tissues in a CX3CL1‐CX3CR1 dependent manner and induce tumour cell apoptosis

2020 ◽  
Vol 14 (10) ◽  
pp. 2546-2559
Author(s):  
Shuo Miao ◽  
Meng Lu ◽  
Yue Liu ◽  
Dan Shu ◽  
Ying Zhu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumour Cell ◽  
Cell Apoptosis ◽  
Dependent Manner

Honokiol Induces Autophagic Apoptosis in Neuroblastoma Cells through a P53-Dependent Pathway

2019 ◽  
Vol 47 (04) ◽  
pp. 895-912 ◽  
Author(s):  
Ming-Chung Lin ◽  
Yuan-Wen Lee ◽  
Yuan-Yun Tseng ◽  
Yung-Wei Lin ◽  
Jui-Tai Chen ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Therapeutic Option ◽  
Neuroblastoma Cells ◽  
Cytochrome C Release ◽  
Dependent Pathway ◽  
Dependent Mechanism ◽  
Stimulation Of

In children, neuroblastomas are the most common and deadly solid tumor. Our previous studies showed that honokiol can cross the blood–brain barrier and kill neuroblastoma cells. In this study, we further evaluated if exposure to honokiol for short periods could induce autophagy and subsequent apoptosis of neuroblastoma cells and possible mechanisms. Exposure of neuroblastoma neuro-2a cells to honokiol for 24[Formula: see text]h induced morphological shrinkage and cell death. As to the mechanisms, honokiol consecutively induced cytochrome c release from mitochondria, caspase-3 activation, DNA fragmentation and cell apoptosis. Separately, honokiol time-dependently augmented the proportion of autophagic cells and the ratio of light chain 3 (LC3)-II/LC3-I. Pretreatment of neuro-2a cells with 3-methyladenine, an inhibitor of autophagy, attenuated honokiol-induced cell autophagy, caspase-3 activation, DNA damage and cell apoptosis. In contrast, stimulation of autophagy by rapamycin, an inducer of autophagy, significantly enhanced honokiol-induced cell apoptosis. Furthermore, honokiol-induced autophagic apoptosis was confirmed in neuroblastoma NB41A3 cells. Knocking down translation of p53 using RNA interference attenuated honokiol-induced autophagy and apoptosis in neuro-2a and NB41A3 cells. Taken together, this study showed that at early periods, honokiol can induce autophagic apoptosis of neuroblastoma cells through activating a p53-dependent mechanism. Consequently, honokiol has the potential to be a therapeutic option for neuroblastomas.

Simulated Ischemia Induces Renal Tubular Cell Apoptosis Through a Nuclear Factor-κB Dependent Mechanism

2002 ◽  
Vol 168 (1) ◽  
pp. 248-252 ◽  
Author(s):  
K.K. Meldrum ◽  
K. Hile ◽  
D.R. Meldrum ◽  
J.A. Crone ◽  
J.P. Gearhart ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Nuclear Factor Κb ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Nuclear Factor ◽  
Simulated Ischemia ◽  
Renal Tubular ◽  
Dependent Mechanism

scholarly journals An apoptosis-driven ‘onco-regenerative niche’: roles of tumour-associated macrophages and extracellular vesicles

2017 ◽  
Vol 373 (1737) ◽  
pp. 20170003 ◽  
Author(s):  
Christopher D. Gregory ◽  
Margaret Paterson
Keyword(s):  
Extracellular Vesicles ◽  
Tumour Cell ◽  
Cell Apoptosis ◽  
Tissue Repair ◽  
B Cell Lymphoma ◽  
Cell Loss ◽  
Endothelial Activation ◽  
Tumour Microenvironment ◽  
Malignant Tumours ◽  
Tissue Repair And Regeneration

The cell-death programme, apoptosis, is well established as a tumour suppressor mechanism. Paradoxically, high levels of apoptosis in tumours are closely coupled with poor prognosis. Indeed, where it has been studied, cell loss is a striking feature of high-grade cancers, illustrating the importance of considering malignant disease as an imbalance between cell gain and cell loss that favours cell gain rather than as a unidirectional disorder of cell gain alone. In addition to orchestrating cell loss, apoptosis can signal regenerative responses—for example compensatory proliferation—in neighbouring cells. Accumulating evidence suggests that normal tissue repair and regenerative processes are hijacked in the malignant tissue microenvironment such that cancer may be likened to a ‘wound that fails to stop repairing’. We have proposed that a critical requirement for the successful growth, progression and re-growth of malignant tumours is a complex milieu, conceptually termed the ‘onco-regenerative niche’, which is composed, in addition to transformed neoplastic cells, of a network of normal cells and factors activated as if in tissue repair and regeneration. Our work is based around the hypothesis that tumour cell apoptosis, macrophage activation and endothelial activation are key, interlinked elements of the onco-regenerative niche and that apoptotic tumour cell–derived extracellular vesicles provide critical intercellular communication vehicles of the niche. In aggressive B-cell lymphoma, tumour cell apoptosis promotes both angiogenesis and the accumulation of pro-tumour macrophages in the lymphoma microenvironment. Furthermore, apoptotic lymphoma-derived extracellular vesicles have potent pro-tumour potential. These findings have important implications for the roles of apoptosis in regulation of malignant diseases and for the efficacy of apoptosis-inducing anti-cancer therapies. This article is part of the discussion meeting issue ‘Extracellular vesicles and the tumour microenvironment’.

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