摘要
Hydrogen sulfide-releasing aspirin (HS-ASA) is a novel compound with potential against cancer. It inhibited the growth of Jurkat T-leukemia cells with an IC50 of 1.9 +/- 0.2 mu M whereas that of ASA was >5000 mu M. It dose-dependently inhibited proliferation and induced apoptosis in these cells, causing a G0/G1 cell cycle arrest. HS-ASA down-regulated beta-catenin protein levels and reduced mRNA and protein expression of beta-catenin/TCF downstream target genes cyclinD1 and c-myc. Aspirin up to 5 mM had no effect on beta-catenin expression. HS-ASA also increased caspase-3 protein levels and dose-dependently increased its activity. These effects were substantially blocked by z-VAD-fmk, a pan-caspase inhibitor.
- 出版日期2013-10