| Objective: Aspirin has been proven to possess definite anticancer effect on colorectal cancer. However, adverse effects including hemorrhage of gastrointestinal tract caused by aspirin limited its clinical usage. Flavonoid is a category of polyphenol that is widespread in plants and food, and possesses various activities such as anticancer activity. Apigenin, a kind of flavonoid, is widely present in vegetables, fruits and tea. It possesses anticancer activity, and has been reported to be able to potentiate the efficacy of anticancer drugs. The present study aimed to observe whether apigenin can enhance the anticancer effect of aspirin and cisplatin and to investigate the underlying mechanism in vitro.Methods:Colorectal cancer cell line HT-29, HCA-7, Moser and DLD-1were selected for research. All cell lines were divided into four groups as follows:the control group, the group treated with10μumol/L apigenin, the group that received aspirin at2.5,5and10mmol/L, the group treated with apigenin and aspirin at varying concentrations. Apigenin was applied2hours prior to addition of aspirin. Cell viability was detected by MTT assay at24,48and72hours post-treatment. Western blot and RT-PCR were performed to detect the effect of different treatment on the expression of COX-2in Moser cells48hours after treating. Protection of IκBα degradation by TNF-a treatment was detected by western blot to validate the effect of apigenin and aspirin against NF-κB activation.Results:Apigenin enhanced the inhibitory effect of aspirin on colorectal cancer cells in a dose-and time-dependent manner. The effect was correlated to suppression on COX-2expression. COX-2expression was inhibited obviously in combined treatment group. In addition, combined treatment resulted in remarkable inhibition of TNF-a-induced degradation of IκBα.Conclusion:Apigenin can potentiate the inhibitory effect of aspirin on colorectal cancer cells through inhibiting COX-2expression. |
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