Abstract
Background: Studies have concentrated on the therapeutic potential of thymoquinone (TQ), a natural polyphenol, in diverse malignancies, such as colorectal cancer. Nevertheless, the precise mechanisms of TQ‐mediated anticancer properties are not yet fully elucidated.Objective: The present study has been designed to scrutinize the impact of TQ on 5‐fluorouracil (5‐FU)–mediated apoptosis in SW‐480 cells.Materials and Methods: SW‐480 cells were treated with TQ, 5‐FU, and a combination of TQ + 5‐FU. MTT assay was employed to assess cell viability. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was applied to evaluate apoptotic markers comprising Bcl‐2, Bax, and caspase‐9 expression levels. The γ‐H2AX protein expression was assessed by western blotting, and Annexin V flow cytometry was implemented to determine the apoptosis rate.Results: 5‐FU significantly reversed the cell proliferation in a dose‐dependent circumstance. The concurrent administration of TQ and 5‐FU led to a substantial inhibition of cell growth in comparison to single treatments (p < 0.05). TQ also facilitated apoptosis via upregulating Bax and caspase‐9 proapoptotic markers and suppressing antiapoptotic mediators, like Bcl‐2. In addition, TQ augmented 5‐FU‐induced apoptosis in SW‐480 cells. 5‐FU, combined with TQ, increased the protein expression of γ‐H2AX in SW‐480 cells compared with groups treated with TQ and 5‐FU alone.Conclusion: The present study’s findings unveil the significance of TQ as a potential therapeutic substance in colorectal cancer, particularly through enhancing 5‐FU‐induced apoptosis.