Aspirin, also known as acetylsalicylic acid, has been shown to have anticancer effects with multiple activities, including inhibition of proliferation, induction of apoptosis, and inhibition of angiogenesis. The functional characteristics and the anti-tumor mechanism of aspirin are largely unknown, except for the suppression of cyclo-oxygenase 2 (COX-2). Aspirin administration is known to associate with lower risks of many cancer types, but less reported in human testicular tumors. We investigated on whether aspirin was able to induce apoptosis in NTera-2 human malignant testicular germ cells, using MTT to detected cell viabilities. The morphological changes, formation of apoptotic bodies, and cell apoptosis were assessed by fluorescence microscopy, Hoechest33342 staining, Annexin V-FITC/PI flow cytometry, RT-PCR and Western blotting were also performed. The result showed that aspirin inhibited the proliferation of NTera-2 cells in a dose- and time-dependent manner, and Fas and caspase-8 were up-regulated. The level of FasL was down-regulated after aspirin treatment. The protein levels of caspase-3, caspase-8, and poly(ADP-Ribose) polymerase (PARP) were increased. Caspase inhibitor Z-VAD-FMK could attenuate the aspirin–induced apoptosis. We concluded that the anticancer activity of aspirin was partially due to the inhibition of cell viability and induction of apoptosis associated with caspase apoptotic pathway.
Key words
aspirin /
NTera-2 cell /
cell apoptosis /
Caspase
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Footnotes
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Funding
Supported by National Natural Science Foundation of China (No.81071696, No.81071656), Project of Changsha Science and Technology Plan（No.K1109006-31）
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