Thymoquinone chemosensitizes colon cancer cells through inhibition of NF-κB

Abstract

In the present study, the effects and molecular mechanisms of thymoquinone (TQ) on colon cancer cells were investigated. Cell viability was determined using a Cell Counting Kit‑8 assay, and the results revealed that treatment with TQ significantly decreased cell viability in COLO205 and HCT116 cells in a dose‑dependent manner. TQ treatment additionally sensitized COLO205 and HCT116 cells to cisplatin therapy in a concentration‑dependent manner. To investigate the molecular mechanisms of TQ action, western blot analysis was used to determine the levels of phosphorylated p65 and nuclear factor‑κB (NF‑κB)‑regulated gene products vascular endothelial growth factor (VEGF), c‑Myc and B‑cell lymphoma 2 (Bcl‑2). The results indicated that TQ treatment significantly decreased the level of phosphorylated p65 in the nucleus, which indicated the inhibition of NF‑κB activation by TQ treatment. Treatment with TQ also decreased the expression levels of VEGF, c‑Myc and Bcl‑2. In addition, the inhibition of NF‑κB activation with a specific inhibitor, pyrrolidine dithiocarbamate, potentiated the induction of cell death and caused a chemosensitization effect of TQ in colon cancer cells. Overall, the results of the present study suggested that TQ induced cell death and chemosensitized colon cancer cells by inhibiting NF‑κB signaling.