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Overview
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Background
Se-Aspirin is a novel selenium-nonsteroidal anti-inflammatory drug (Se-NSAID) [1]. NSAIDs have demonstrated intestinal antineoplastic effects in various animal intestinal cancer models. Selenium (Se) compounds have attracted a vast interest as promising chemo-preventive agents. Several epidemiological studies have reported an inverse association between the nutritional Se status and cancer risk. Se functioned as chemo-preventive agent for cancer therapy in the past few years. Se-Aspirin was a hybrid of selenium and a nonsteroidal anti-inflammatory drug. t Se-Aspirin reduced the viability of different cancer cell lines, particularly colorectal cancer (CRC) cells with the IC50 value of 3.4 μM. Se-Aspirin inhibited the cell cycle in G1 and G2/M phases and induced apoptosis by activating caspase 3/7 and PARP cleavage. Long-term exposure to Se-Aspirin has been reported to cause an increase in intracellular reactive oxygen species levels in CRC cells [1].
Reference:[1] Plano D, Karelia D N, Pandey M K, et al. Design, synthesis, and biological evaluation of novel selenium (Se-NSAID) molecules as anticancer agents[J]. Journal of medicinal chemistry, 2016, 59(5): 1946-1959.
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