Crocetin Induces Cytotoxicity in Colon Cancer Cells Via p53-independent Mechanisms


Objective: Crocin has been proposed as a promising candidate for cancer chemoprevention. The purpose ofthis investigation was to investigate the chemopreventive action and the possible mechanisms of crocin againsthuman colon cancer cells in vitro.
Methods: Cell proliferation was examined using MTT assay and the cell cycledistribution fractions were analyzed using fow cytometric analysis after propidium iodide staining. Apoptosiswas detected using theTUNEL Apoptosis Detection Kit with laser scanning confocal microscope. DNA damagewas assessed using the alkaline single-cell gel electrophoresis assay, while expression levels of p53, cdk2, cyclinAand P21 were examined by Western blot analysis.
Results: Treatment of SW480 cells with crocetin (0.2, 0.4,0.8 mmol/L) for 48 h signifcantly inhibited their proliferation in a concentration-dependent manner. Crocetin(0.8 mmol/L) signifcantly induced cell cycle arrest through p53-independent mechanisms accompanied by P21induction. Crocetin (0.8 mmol/L) caused cytotoxicity in the SW480 cells by enhancing apoptosis and decreasingDNA repair capacity in a time-dependent manner.
Conclusions: This report provides evidence that crocetin isa potential anticancer agent, which may be used as a chemotherapeutic drug.