| Literature DB >> 23896061 |
Mitali Chattopadhyay1, Niharika Nath, Ravinder Kodela, Tomasz Sobocki, Shalaka Metkar, Zong Yuan Gan, Khosrow Kashfi.
Abstract
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 μM whereas that of ASA was >5000 μM. It dose-dependently inhibited proliferation and induced apoptosis in these cells, causing a G₀/G₁ cell cycle arrest. HS-ASA down-regulated β-catenin protein levels and reduced mRNA and protein expression of β-catenin/TCF downstream target genes cyclinD1 and c-myc. Aspirin up to 5 mM had no effect on β-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.Entities:
Keywords: ALL; ASA; Apoptosis; CML; Caspase-3; Cell cycle; Chronic Myeloid Leukemia; HS-ASA; Hydrogen sulfide; Leukemia; NO; NSAIDs; Proliferation; acute lymphoblastic leukemia; aspirin; hydrogen sulfide-releasing aspirin; nitric oxide; nonsteroidal anti-inflammatory drugs; β-Catenin
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Year: 2013 PMID： 23896061 PMCID： PMC3769470 DOI： 10.1016/j.leukres.2013.07.004
Source DB: PubMed Journal: Leuk Res ISSN： 0145-2126 Impact factor: 3.156