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Nonsteroidal anti-inflammatory drugs such as acetylsalicylic Pemetrexed (aspirin; ASA) have been known to induce apoptosis or inhibit proliferation of a variety of human cancer cells including those of colon [11], lung [12], stomach [13], and breast [14]. Several mechanisms have been proposed for the aspirin-induced cellular apoptosis, for example, up-regulation of several proapoptotic proteins [15], down-regulation of cell death inhibitors [15] and [16], and inhibition of NF-κB activity [15] and [17]. However, so far, little has been reported regarding the effect of aspirin on STAT3 signaling in human tumor cells.
Here, we report that aspirin induces the apoptosis of human glioblastoma cells and suggest the role of aspirin as an inhibitor of IL-6-IL-6R-STAT3 signaling pathway.
Materials and methods
Chemical and reagent. Aspirin, protease inhibitor cocktail, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) were purchased from Sigma. Recombinant human IL-6 was obtained from R&D system. Mouse monoclonal anti-Bcl-2, Cyclin D1 and p21 antibodies, and rabbit polyclonal anti-STAT3, XIAP, and PARP antibodies were from Santa Cruz biotechnology. Rabbit polyclonal anti-pSTAT3 and mouse monoclonal anti-α-Tubulin antibodies were obtained from Cell Signaling and Biogenex, respectively. FITC-conjugated donkey anti-rabbit IgG was purchased from Jackson Immunoresearch.