BAX Expression in Colorectal Cancer Cells Exposed to Aspirin and Novel Aspirin Analogues

Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) have long been used in the treatment of colorectal cancer and other neoplasm whose underlying efficacy and biomolecular mechanism is generally believed to be through induction of Bax protein among others resulting in cell apoptosis but its toxicity precludes its chemotherapeutic benefits. However, there exists a dearth of knowledge on the use of other more efficacious and more tolerable novel aspirin analogues with better prognosis. The purpose of this study was to investigate Bax induction on SW480 cells treated with 0.5mM aspirin and novel aspirin analogues; PN508 (bis-carboxylphenol-succinate), PN517 (Fumaroyldiasprin) and PN529 (Isopropyl m- bromobenzoylsalicylate) measured after 48 hours of incubation at 370C using analytical digital photomicroscopy. The results of this study showed a 60-70% folds increase in Bax expression in 0.5mM Aspirin treated cells. 0.5mM PN517 and PN529 treated cells showed 70-80% folds increases in Bax expression whilst 0.5mM PN508 treated cells showed a significance of 100-120% folds increase in Bax expression. This study reports that 0.5mM aspirin and novel aspirin analogues PN508, PN517 and PN529 caused increase in Bax expression when exposed to SW480 cells at 370C for 48 hours. It could be inferred from the results of this study that novel aspirin analogues PN508, PN517 and PN529 are potentially more potent inducers of Bax protein than aspirin in SW480 cells. We therefore recommend that these novel aspirin analogues be considered in designing alternative and more efficacious drugs for the treatment of colorectal cancer and other neoplasm in the nearest future.