scholarly journals Matrine-induced autophagy regulated by p53 through AMP-activated protein kinase in human hepatoma cells

2015 ◽  
Vol 47 (2) ◽  
pp. 517-526 ◽  
Author(s):  
SHAN-BU XIE ◽  
XING-XING HE ◽  
SHU-KUN YAO
Keyword(s):  
Protein Kinase ◽  
Hepatoma Cells ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Amp Activated Protein Kinase

Celecoxib-induced increase in cytosolic Ca2+ levels and apoptosis in HA59T human hepatoma cells

2014 ◽  
Vol 33 (11) ◽  
pp. 1089-1098
Author(s):  
H-H Cheng ◽  
C-T Chou ◽  
Y-C Lu ◽  
T Lu ◽  
C-C Chi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Phospholipase C ◽  
Hepatoma Cells ◽  
Dependent Manner ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Fura 2 ◽  
Kinase C

Celecoxib has been shown to have antitumor effect in previous studies but the mechanisms are unclear. The effect of celecoxib on cytosolic Ca2+ concentrations ([Ca2+]i) and viability in HA59T human hepatoma cells was explored. The Ca2+-sensitive fluorescent dye fura-2 was applied to measure [Ca2+]i. Celecoxib at concentrations of 10–50 μM induced a [Ca2+]i rise in a concentration-dependent manner. The response was reduced by 80% by removing Ca2+. Celecoxib induced Mn2+ influx, leading to quenching of fura-2 fluorescence. Celecoxib-evoked Ca2+ entry was suppressed by nifedipine, econazole, SK&F96365, and protein kinase C modulators. In the absence of extracellular Ca2+, incubation with the endoplasmic reticulum Ca2+ pump inhibitor thapsigargin nearly abolished celecoxib-induced [Ca2+]i rise. Incubation with celecoxib abolished thapsigargin-induced [Ca2+]i rise. Inhibition of phospholipase C with U73122 abolished celecoxib-induced [Ca2+]i rise. At 1–50 μM, celecoxib inhibited cell viability by less than 20%, which was not reversed by chelating cytosolic Ca2+ with 1,2-bis(2-aminophenoxy)ethane-N, N, N′, N′-tetraacetic acid/acetoxy methyl (BAPTA/AM). Celecoxib (10–50 μM) also induced apoptosis. In sum, in HA59T hepatoma cells, celecoxib induced a [Ca2+]i rise by evoking phospholipase C-dependent Ca2+ release from the endoplasmic reticulum and Ca2+ entry via protein kinase C-sensitive store-operated Ca2+ channels. Celecoxib also caused cell death via apoptosis.

Sign in / Sign up

Export Citation Format

Share Document