Colorectal cancer (CRC) is a major cause of mortality and morbidity. Chronic inflammation is closely associated with the development, progression and prognosis of the majority of intestinal malignancies. In recent years, targeting the nuclear factor (NF)‑κB signaling pathway for CRC therapy has become an attractive strategy. Riccardin D, a novel macrocyclicbis (bibenzyl) compound, was isolated from the Chinese liverwort plant. Previous studies have suggested that Riccardin D exerted chemo‑preventative effects against the intestinal malignancy formation. In the present study, cell counting kit‑8, Hochest 33258 staining, mitochondria membrane permeability assay, western blotting analysis, reverse transcription‑polymerase chain reaction, luciferase reporter gene assay and molecular modeling analysis were performed to detect the effect and mechanisms of Riccardin D on human colon cancer cells. The results demonstrated that Riccardin D significantly inhibited the growth of HT‑29 cells. In addition, the cDNA expression of cyclooxygenase‑2, and the protein expression and activity of NF‑κB and tumor necrosis factor‑α were downregulated; however, the protein expression of cleaved caspase‑3 and ‑9, and cleaved poly (adenosine diphosphate‑ribose) polymerase, and the B‑cell lymphoma (Bcl)‑2: Bcl‑2‑associated X protein ratio were upregulated. Furthermore, Auto Dock analysis identified binding sites between Riccardin D and NF‑κB. These results indicated that Riccardin D may inhibit cell proliferation and induce apoptosis in HT‑29 cells, which may be associated with the blocking of the NF‑κB signaling pathway. Thus, Riccardin D should be investigated as an NF‑κB inhibitor in cancer therapy.
Keywords: colorectal cancer; Riccardin D; nuclear factor-κB signaling; autodock analysis.