Caffeine induces matrix metalloproteinase-2 (MMP-2) and MMP-9 down-regulation in human leukemia U937 cells via Ca2+/ROS-mediated suppression of ERK/c-fos pathway and activation of p38 MAPK/c-jun pathway

2010 ◽  
Vol 224 (3) ◽  
pp. 775-785 ◽  
Author(s):  
Wen-Hsin Liu ◽  
Long-Sen Chang
Keyword(s):  
Matrix Metalloproteinase ◽  
P38 Mapk ◽  
Matrix Metalloproteinase 2 ◽  
Human Leukemia ◽  
U937 Cells ◽  
Down Regulation

scholarly journals Down-regulation of glomerular matrix metalloproteinase-2 gene in human NIDDM

Diabetologia ◽  
1997 ◽  
Vol 40 (12) ◽  
pp. 1449-1454 ◽  
Author(s):  
D. Del Prete ◽  
F. Anglani ◽  
M. Forino ◽  
M. Ceol ◽  
P. Fioretto ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 2 ◽  
Down Regulation

Crosstalk Between Human Monocytic U937 Cells and Gingival Fibroblasts in Coculturally Enhanced Matrix Metalloproteinase-2 Expression

2016 ◽  
Vol 87 (10) ◽  
pp. 1228-1237 ◽  
Author(s):  
Po-Jan Kuo ◽  
Hsiao-Lun Lin ◽  
Chi-Yu Lin ◽  
Yu-Tang Chin ◽  
Hsiao-Pei Tu ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 2 ◽  
U937 Cells ◽  
Gingival Fibroblasts

scholarly journals Naja atra Cardiotoxin 1 Induces the FasL/Fas Death Pathway in Human Leukemia Cells

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2073
Author(s):  
Jing-Ting Chiou ◽  
Liang-Jun Wang ◽  
Yuan-Chin Lee ◽  
Long-Sen Chang
Keyword(s):  
P38 Mapk ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Human Leukemia ◽  
U937 Cells ◽  
Fasl Expression ◽  
Mechanistic Pathway ◽  
Leukemia Cell Lines ◽  
Sirna Knockdown ◽  
Naja Atra

This study aimed to investigate the mechanistic pathway of Naja atra (Taiwan cobra) cardiotoxin 1 (CTX1)–induced death of leukemia cell lines U937 and HL-60. CTX1 increased cytoplasmic Ca2+ and reactive oxygen species (ROS) production, leading to the death of U937 cells. It was found that Ca2+-induced NOX4 upregulation promoted ROS-mediated p38 MAPK phosphorylation, which consequently induced c-Jun and ATF-2 phosphorylation. Using siRNA knockdown, activated c-Jun and ATF-2 were demonstrated to regulate the expression of Fas and FasL, respectively. Suppression of Ca2+-mediated NOX4 expression or ROS-mediated p38 MAPK activation increased the survival of U937 cells exposed to CTX1. FADD depletion abolished CTX1-induced cell death, caspase-8 activation, and t-Bid production, supporting the correlation between the Fas death pathway and CTX1-mediated cytotoxicity. Among the tested N. atra CTX isotoxins, only CTX1 induced Fas and FasL expression. Chemical modification studies revealed that intact Met residues were essential for the activity of CTX1 to upregulate Fas and FasL expression. Taken together, the data in this study indicate that CTX1 induces c-Jun-mediated Fas and ATF-2-mediated FasL transcription by the Ca2+/NOX4/ROS/p38 MAPK axis, thereby activating the Fas death pathway in U937 cells. Furthermore, CTX1 activates Fas/FasL death signaling in the leukemia cell line HL-60.

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
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