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.