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Non steroidal anti-inflammatory drugs (NSAID) such as aspirin have chemopreventive activity against colorectal tumors. Although the molecular mechanism has not been fully established, it is thought to involve COX-mediated carcinogen activation, cell proliferation, apoptosis and immune surveillance. In the present study, the effect of aspirin on the expression of survivin and COX-2 and their possible correlation in induced colorectal carcinoma were investigated. We used 1, 2 dimethylhydrazine (DMH) for induction of aberrant crypt foci (ACF) that contribute to the stepwise progression to colorectal cancer. The rats were divided into 3 groups; control group, DMH group and DMH with aspirin group. The expression of survivin and COX-2 was investigated through IHC and immunoblot and the correlation in both DMH-induced lesions and after aspirin treatment was evaluated. It was found that aspirin has the ability to reduce the incidence of the ACF when it was given as a chemopreventive and it was found that both survivin and COX-2 are overexpressed in ACF compared to normal group. They seem to be early events in the occurrence of colorectal carcinoma. In the evaluation to the effect of aspirin it was found that aspirin significantly causes down-regulation of both survivin and COX-2 (P=0.0001). Furthermore, we found survivin and COX-2 to be positively correlated in ACF lesion and after aspirin treatment (r = 0.816 and r = 0.742) respectively. All of these findings suggested that targeted therapies against survivin and COX-2 may be valuable in chemoprevention of colorectal carcinoma.

The Effect of Aspirin on Survivin and COX-2 Expression and Their Correlation in Aberrant Crypt Foci