Rosmarinic acid sensitizes cell death through suppression of TNF-α-induced NF-κB activation and ROS generation in human leukemia U937 cells

2010 ◽  
Vol 288 (2) ◽  
pp. 183-191 ◽  
Author(s):  
Dong-Oh Moon ◽  
Mun-Ock Kim ◽  
Jae-Dong Lee ◽  
Yung Hyun Choi ◽  
Gi-Young Kim
Keyword(s):  
Cell Death ◽  
Rosmarinic Acid ◽  
Ros Generation ◽  
Human Leukemia ◽  
U937 Cells ◽  
Tnf Α

scholarly journals Naja atra Cardiotoxin 3 Elicits Autophagy and Apoptosis in U937 Human Leukemia Cells through the Ca2+/PP2A/AMPK Axis

Toxins ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 527 ◽  
Author(s):  
Jing-Ting Chiou ◽  
Yi-Jun Shi ◽  
Liang-Jun Wang ◽  
Chia-Hui Huang ◽  
Yuan-Chin Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Membrane Damage ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
U937 Cells ◽  
Cell Membrane Damage ◽  
Human Leukemia Cells ◽  
Phosphatase 2A ◽  
Induced Apoptosis ◽  
Naja Atra

Cardiotoxins (CTXs) are suggested to exert their cytotoxicity through cell membrane damage. Other studies show that penetration of CTXs into cells elicits mitochondrial fragmentation or lysosome disruption, leading to cell death. Considering the role of AMPK-activated protein kinase (AMPK) in mitochondrial biogenesis and lysosomal biogenesis, we aimed to investigate whether the AMPK-mediated pathway modulated Naja atra (Taiwan cobra) CTX3 cytotoxicity in U937 human leukemia cells. Our results showed that CTX3 induced autophagy and apoptosis in U937 cells, whereas autophagic inhibitors suppressed CTX3-induced apoptosis. CTX3 treatment elicited Ca2+-dependent degradation of the protein phosphatase 2A (PP2A) catalytic subunit (PP2Acα) and phosphorylation of AMPKα. Overexpression of PP2Acα mitigated the CTX3-induced AMPKα phosphorylation. CTX3-induced autophagy was via AMPK-mediated suppression of the Akt/mTOR pathway. Removal of Ca2+ or suppression of AMPKα phosphorylation inhibited the CTX3-induced cell death. CTX3 was unable to induce autophagy and apoptosis in U937 cells expressing constitutively active Akt. Met-modified CTX3 retained its membrane-perturbing activity, however, it did not induce AMPK activation and death of U937 cells. These results conclusively indicate that CTX3 induces autophagy and apoptosis in U937 cells via the Ca2+/PP2A/AMPK axis, and suggest that the membrane-perturbing activity of CTX3 is not crucial for the cell death signaling pathway induction.

scholarly journals Induction of Programmed Cell Death by Parvovirus H-1 in U937 Cells: Connection with the Tumor Necrosis Factor Alpha Signalling Pathway

1998 ◽  
Vol 72 (11) ◽  
pp. 8893-8903 ◽  
Author(s):  
Béatrice Rayet ◽  
José-Antonio Lopez-Guerrero ◽  
Jean Rommelaere ◽  
Christiane Dinsart
Keyword(s):  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Cell Line ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
U937 Cells ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The human promonocytic cell line U937 undergoes apoptosis upon treatment with tumor necrosis factor alpha (TNF-α). This cell line has previously been shown to be very sensitive to the lytic effect of the autonomous parvovirus H-1. Parvovirus infection leads to the activation of the CPP32 ICE-like cysteine protease which cleaves the enzyme poly(ADP-ribose)polymerase and induces morphologic changes that are characteristic of apoptosis in a way that is similar to TNF-α treatment. This effect is also observed when the U937 cells are infected with a recombinant H-1 virus which expresses the nonstructural (NS) proteins but in which the capsid genes are replaced by a reporter gene, indicating that the induction of apoptosis can be assigned to the cytotoxic nonstructural proteins in this cell system. The c-Myc protein, which is overexpressed in U937 cells, is rapidly downregulated during infection, in keeping with a possible role of this product in mediating the apoptotic cell death induced by H-1 virus infection. Interestingly, four clones (designated RU) derived from the U937 cell line and selected for their resistance to H-1 virus (J. A. Lopez-Guerrero et al., Blood 89:1642–1653, 1997) failed to decrease c-Myc expression upon treatment with differentiation agents and also resisted the induction of cell death after TNF-α treatment. Our data suggest that the RU clones have developed defense strategies against apoptosis, either by their failure to downregulate c-Myc and/or by activating antiapoptotic factors.

The Association Between p38 MAPK-Mediated TNF-α/TNFR2 up-Regulation and 2-(4-Aminophenyl)-7-Methoxybenzothiazole-Induced Apoptosis in Human Leukemia U937 Cells

2015 ◽  
Vol 231 (1) ◽  
pp. 130-141 ◽  
Author(s):  
Chia-Hui Huang ◽  
Ying-Jung Chen ◽  
Tzu-Yu Chao ◽  
Wen-Hsin Liu ◽  
Jung-Jung Changchien ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Human Leukemia ◽  
U937 Cells ◽  
Tnf Α ◽  
Induced Apoptosis

Taiwan cobra phospholipase A2 suppresses ERK-mediated ADAM17 maturation, thus reducing secreted TNF-α production in human leukemia U937 cells

Toxicon ◽  
2014 ◽  
Vol 86 ◽  
pp. 79-88 ◽  
Author(s):  
Ying-Jung Chen ◽  
Hui-Chen Lin ◽  
Ku-Chung Chen ◽  
Shinne-Ren Lin ◽  
Tian-Lu Cheng ◽  
...  
Keyword(s):  
Phospholipase A2 ◽  
Human Leukemia ◽  
U937 Cells ◽  
Tnf Α
Sign in / Sign up

Export Citation Format

Share Document