Downregulation of Bcl-2 Family Expression and Enhanced DNA Fragmentation in HCT116 by Thymoquinone

Background Nigella sativa is the source of thymoquinone (TQ), an active phenolic compound with numerous pharmacological properties, including anti-tumor, anti-angiogenic, and antioxidant activities. Nevertheless, the mechanism by which TQ exerts its therapeutic effects and its potential utility in cancer treatment remain largely unknown. Purpose This study examine the potential anticancer properties of TQ at a concentrations of 8, 12, and 16 µg in colon cancer cells (HCT116). Materials and Methods We investigated the effects of TQ in promoting apoptosis and inhibiting cell proliferation in colon cancer cells (HCT116) in the present study. It showed that in TQ-treated HCT116 cells, antioxidant levels (superoxide dismutase, catalase and glutathione) were reduced in a dose-dependent manner (8, 12, and 16 µg), and that TQ significantly increased the production of reactive oxygen species, lipid peroxidation in terms of malondialdehyde, and loss of cell viability. Results Additionally, morphological changes and DNA fragmentation confirm that TQ induces oxidative stress-mediated apoptosis. Additionally, TQ treatment effectively increases the expression of Bax, caspase-9, and caspase-3 while decreasing the expression of Bcl-2 and Bcl-xl in colon cancer cells. Conclusion Our findings collectively demonstrate that TQ’s anti-tumor effects in HCT116 colon cancer cells reduce cell proliferation and promote apoptosis by modifying pro- and anti-apoptotic molecular events. Our results suggest that TQ could be utilized as a therapeutic agent to treat colon cancer.