کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2515841 | 1118562 | 2011 | 7 صفحه PDF | دانلود رایگان |

Extracellular adenosine significantly reduced cell viability in a dose (0.1–20 mM)- and treatment time (24–72 h)-dependent manner in GT3-TKB cells, a human gastric cancer cell line. Nuclei of cells were reactive to Hoechst 33342, a marker of apoptosis, and an anti-single-stranded DNA. Adenosine-induced GT3-TKB cell death was significantly inhibited by dipyridamole, an inhibitor of adenosine transporter, and 5′-amino-5′-deoxyadenosine, an inhibitor of adenosine kinase, but the effect was not affected by theophylline, a broad inhibitor of adenosine receptors, 8-cyclopentyltheophylline, an inhibitor of A1 adenosine receptors or 3,7-dimethyl-1-propargylxanthine, an inhibitor of A2a adenosine receptors. Adenosine had no effect on mitochondrial membrane potentials. The effect of adenosine on GT3-TKB cell death was not inhibited by a pancaspase inhibitor or inhibitors of caspase-1,-3,-4,-8, and -9. 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAR), an activator of AMP-activated protein kinase (AMPK), significantly reduced GT3-TKB cell viability, but the AICAR action was not reinforced in the presence of adenosine. The results of the present study, thus, suggest that extracellular adenosine induces apoptosis in GT3-TKB cells by its uptake into cells and conversion to AMP followed by activation of AMPK, regardless of caspase activation linked to the mitochondria and the endoplasmic reticulum.
Journal: Biochemical Pharmacology - Volume 67, Issue 10, 15 May 2004, Pages 2005–2011