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Aspirin has several beneficial pharmacological properties and recently was reported to have anti-neoplastic properties, shown by epidemiological studies on colorectal cancer. Aspirin also inhibited cell proliferation and induced apoptosis in a number of cancer cell lines in vitro. This anti-proliferative and apoptotic effect is considered to be an important mechanism for the anti-tumor activity of aspirin. Several molecular mechanisms underlying the apoptotic effect of aspirin in regulating tumor cell growth have been reported. These include the inhibition of cyclooxygenases (COX-1 and COX-2), thus depressing prostaglandin synthesis, often over-expressed in cancers. COX-independent mechanisms involve activation of p38 mitogen-activated protein kinase (p38 MAPK) in human fibroblasts, inhibition of human telomerase reverse transcriptase in colon cancer cells, and increase in protein expression of p53 in the human oral cancer cell line OC2. The release of cytochrome c is reported in several cancer cell lines, together with the activation of caspases and cleavage of poly (ADP-ribose) polymerase (PARP). The up-regulation of Bak and Bax was observed in gastric and colon cell lines, whereas down-regulation of Bcl-2 and Bcl-xL occurred in colon cancer cells. Aspirin also down-regulated cytosolic phospholipase A2 mRNA expression in colon cancer cells, induced apoptosis by increasing intracellular H202 level in human hepatoma-derived SKHep-1 cells and altered the signaling pathway of the transcription factor NF-kB in gastric cells. We studied the effect of aspirin on the yeast Saccharomyces cerevisiae, when grown on fermentable and non …