Differential effect of psoralidin in enhancing apoptosis of colon cancer cells via nuclear factor-κB and B-cell lymphoma-2/B-cell lymphoma-2-associated X protein signaling pathways.

Worldwide, colon cancer is the third most common cancer in terms of incidence, following lung and breast cancer. Resistance to psoralidin frequently occurs following its use as an anticancer treatment. However, the mechanisms underlying the effects of psoralidin on colon cancer, remain to be elucidated. Hence, the present study investigated the anticancer effects and potential mechanism of action of psoralidin on SW480 human colon cancer cells. In the present study, an MTT assay was performed to measure the viability of SW480 cells. Additionally, an Annexin V-fluorescein isothiocyanate/propidium iodide apoptosis detection kit, DAPI staining assay and caspase-3 colorimetric assay kits were used to analyze the cellular apoptosis of SW480 cells. The nuclear factor-κB (NF-κB) p65 activity and B-cell lymphoma-2 (Bcl-2)/Bcl-2-associated X protein (Bax) protein expression of SW480 cells was detected using NF-κB colorimetric assay kits and western blot analysis, respectively. Bcl-2 inhibitor ABT-737 was added to SW480 cells and the subsequent effects and mechanism of action of psoralidin on SW480 colon cancer cells was studied. In the present study, psoralidin reduced SW480 cell viability and enhanced the cellular apoptosis of SW480 cells in a dose-dependent manner. Caspase-3 activity of SW480 cells was increased following treatment with psoralidin. Additionally, psoralidin was able to reduce the NF-κB p65 activity of SW480 cells. Furthermore, psoralidin was able to reduce Bcl-2 protein expression and increase Bax protein expression in SW480 cells. Notably, Bcl-2 inhibitor was observed to enhance the effects of psoralidin on SW480 cells. The results of the present study suggest that psoralidin may be a candidate drug for the treatment of colon cancer by inhibition of the NF-κB and Bcl-2/Bax signaling pathways.